2014 Curs Nefrologie-De Prezentat 4-Ian 2014

8/12/2019 2014 Curs Nefrologie-De Prezentat 4-Ian 2014

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Titu Maiorescu University

Curs Medicina Interna

NEPHROLOGY- I

Prof univ dr Ion C Tintoiu


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Characteristics of Renal Structure andFunction

I. Physiological Anatomy of the Kidney


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Renal cortex

Cortical lobules - whichform caps over the

bases of the pyramids Renal columns - which

dip in between thepyramids

Renal medulla

has 10 conical massescalled renal pyramids,their apices form renalpapillae

Renal sinus

Space that extends into kidney from hilus

Contains branches of renal artery and renal vein

Renal pelvis divides into 2-3 major calices and these in turn divide into 7-13 minor calices, each minor calyx (cup of flower) ends in an expansion

which is indented by 1-3 renal papillae


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Histologically, each kidney is composed 1-3 millionuriniferous tubules.Each consists of

Secretory part - which forms urine is callednephron, functional unit of kidney Nephrons open in to collecting tubules. Many such tubules

unite to form the ducts of Bellini which open into minorcalices

Arterial Supply

One renal artery on each side arising from abdominalaorta

At or near hilus, renal artery divides into anterior andposterior branches giving rise to segmental arteries

Lymphatics

Lateral aortic nodes


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Major Functions of the Kidneys

1. Regulation of:

-body fluid osmolarity and volume-electrolyte balance

-acid-base balance

-blood pressure

2. Excretion of

. metabolic products,drugs

.foreign substances (pesticides, chemicals etc.)

.excess substance (water, etc)

3. Secretion of

-erythropoitin

-1,25-dihydroxy vitamin D3(vitamin D activation)

- renin- rosta landin


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-Nephron struc

and

Functions

Glomerulus

Proximal Tubule (PCT)

Loop of Henle

Distal tubule

Collecting tubule


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Functions of the Nephron

Filtration

Reabsorption Secretion

Excretion


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Glomerular Filtration

Figure 26.10a, b


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Proximal Tubule (PCT)Reabsorption

NaCl

Water

Bicarbonate

Glucose Proteins

Aminoacids

K+, Mg, PO4+, uric acid,

ureaSecretion

Organic anions

Organic cations

Ammonia products

Reabsorption of solutes in PCT


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Loop of Henle 25-30% ultrafiltrate reaches loop of Henle

15-20% filtered Na+load reabsorbed Solute and water reabsorption is passive and follows

concentration and osmotic gradients (except thick

ascending loop) Sodium reabsorption is coupled to both K+and Cl-

reabsorption Cl-in tubular fluid is rate limiting factor

Calcium and magnesium reabsorption Parathyroid hormone calcium reabsorption at this

site Loop diuretics inhibit Na and Cl reabsorption in TAL

compete with Cl- for its binding site on carrier protein


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Distal tubule

Very tight junctions between tubular cellsrelatively impermeable to water and Na+

5% of filtered Na+load reabsorbed

Parathyroid hormone and vit D mediatedcalcium reabsorption

The late distal segment (collecting segment) Hormone mediated Ca+reabsorptionAldosterone mediated Na+reabsorption


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Collecting tubule

5-7% of filtered Na+load is reabsorbed

Cortical collecting tubule

two types ofcells:Principal cellssecrete K+aldosterone

mediated Na

+

reabsorptionIntercalated cellsacid base regulation


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A Summary of Renal Function


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Nephron symphony


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.Renal Pathology


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Diseases of the kidney

1-Glomeruli

Glomerulonephritis

Primary

Secondary

Chronic

2-Tubulointerstitium

Acute tubularnecrosis

Pyelonephritis

Acute

chronic

3-Vessels

Nephrosclerosis

4-Urinary obstruction

Stones

Hydronephrosis

5- Cystic diseases of thekidney

6-Tumors

BenignMalignan

7-Litiazis


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.Glomerular diseases


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GLOMERULONEPHRITIS

Acute Glomerulonephritis:

Rapidly Progressive

Glomerulonephritis Chronic Glomerulonephritis

Nephrotic Syndrome

Asymptomatic urinary

abnormalities


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Glomerular disease

Primary Glomerulonephritis

Minimal change GN

Membranous GN

Focal segmental GS

Membranoproliferative GN

Diffuse proliferative GN

Crescentic GN Seconday

SLE, DM, Amyloidosis, Goodpasture, vasculitis

Hereditary

Albort syndrome


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Glomerular diseases:

Primary Glomerulonephritis


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.AcuteGlomerulonephritis


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Acute glomerulonephritis is theinflammation of the glomeruliwhich causesthe kidneys to malfunction

It is also called Acute Nephritis,Glomerulonephritis and Post-StreptococcalGlomerulonephritis

Predominantly affects children from ages 2to 12

Incubation period is 2 to 3 weeks

Acute GlomerulonephritisDefinition


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Fever

Headache

Malaise

Anorexia

Nausea and vomiting

High blood pressure

Pallor due to edema and/or anemia Confusion

Lethargy

Loss of muscle tissue

Enlargement of the liver

Acute GlomerulonephritisGeneral Symptoms


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Hematuria:dark brown or smoky urine

Oliguria: urine output is < 400 ml/day

Edema: starts in the eye lids and facethen the lower and upper limbs then

becomes generalized; may be migratory

Hypertension: usually mild to moderateHypoproteinemia,

hypercholesterolemia),

mixed

Acute Glomerulonephritis

Signs and Symptoms


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Acute GlomerulonephritisEtiology

Infectious

Streptococcal

Nonstreptococcal postinfectious

glomerulonephritis

Bacterial

Viral

Parasitic

Noninfectious

Multisystem systemic diseases

Primary glomerular diseases


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INVESTIGATIONSBase line measurements:- Urea

- reatinine-Urinalysis MSU):a) Urine microscopy red cell cast)

b) proteinuria


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Hypertensive encephalopathy,

Heart failure and acute

Pulmonary edema may occur in severecases

Acute renal necrosis due to injury of

capillary or capillary thrombosis


Complications

A t Gl l h iti


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proper hygiene

prompt medical assessment fornecessary antibiotic therapy should be

sought when infection is suspected

prophylactic immunizations


Prevention


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.Chronic glomerulonephritis


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Chronic glomerulonephritis

The condition is characterized

1 - irreversible and progressive glomerularand tubulointerstitial fibrosis

2-ultimately leading to a reduction in theglomerular filtration rate (GFR) and

3- retention of uremic toxins

.. The diagnosis of CKD can be made withoutknowledge of the specific cause.



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Etiology

Nearly all forms of acute glomerulonephritishave atendency to progress to chronicglomerulonephritis.

The progression from acute glomerulonephritis to

chronic glomerulonephritis is variable.

Whereas complete recovery of renal function is therule for patients with poststreptococcal

glomerulonephritis, several otherglomerulonephritides, such asimmunoglobulin A (IgA) nephropathy, oftenhave a relatively benign course and many do notprogress to ESRD.

Ch i l l h iti


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Pathogenesis

Reduction in nephron mass from the initial injuryreduces the GFR.

This reduction leads to hypertrophy andhyperfiltration of the remaining nephrons and to

the initiation of intraglomerular hypertension.These changes occur in order to increase the GFR of

the remaining nephrons, thus minimizing thefunctional consequences of nephron loss.

The changes, however, are ultimately detrimentalbecause they lead to glomerulosclerosis andfurther nephron loss.



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Histo log ic Findings

In early stages, the glomeruli may still

show some evidence of the primary

disease.

In advanced stages, the glomeruli are

hyalinized and obsolescent.

The tubules are disrupted and atrophic,and marked interstitial fibrosis and

arterial and arteriolar sclerosis occur.



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Histo log ic Find ings

1-Min imal-Change Disease

2-Focal segmentalg lomerulosc leros is

3-Mesang iocap i l lary GN

4-Membranous neph ropathy


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Mesangial proli ferativeMPGN

1-Hypercellularity,

2-Mesangial proliferation,3-Inflammatory cell infiltrate,

4-Positive IF for IgG and C3 and

5-Subepithelial deposits on EM.


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Chronic g lomerulonephr i t is


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Clinical Manifestations

Uremia-specific findings Edemas

Hypertension

Jugular venous distension (if severe volumeoverload is present)

Pulmonary rales (if pulmonary edema ispresent)

Pericardial friction rub in pericarditis Tenderness in the epigastric region or blood

in the stool (possible indicators for uremicgastritis or enteropathy)



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Lab Stud ies

Urinalysis

Urinary protein excretion

Serum chemistry

Serum creatinine and urea nitrogen levelsare elevated.

Impaired excretion of potassium, free water, andacid results in hyperkalemia, hyponatremia, andlow serum bicarbonate levels, respectively.

Impaired vitamin D-3 production results inhypocalcemia, hyperphosphatemia, and high levelsof parathyroid hormone.

Low serum albumin levels may be present ifuremia interferes with nutrition or if the patient isnephrotic.


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Chron ic glomeruloneph r i tis


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g p

Treatment

Minimal change glomerulonephritis

1-Corticosteroidsinduce remission in >90% of

children and 80% of adults (slower response).

2-immunosuppression:(cyclophosphamide,

ciclosporin (=cylosporin)): early/ frequent

relapses; steroid SEs/dependence.Prognosis: 1% progress to ESRF.



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Treatment

Focal segmental glomerulosclerosis

Poor response to corticosteroids(10

30%). Cyclophosphamide or ciclosporin

(=cylosporin) may be used in steroid-resistant

cases.

Prognosis: 3050% progress to ESRF.



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Treatment

Mesangial proliferative GN

1-Antibiotics,

2-Diuretics, and3-Antihypertensives as necessary.

4-Dialysis is rarely required.

Prognosis: Good.



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Treatment

Membranous nephropathy

If renal function deteriorates, consider

corticosteroids and chlorambucil.

Prognosis:Untreated, 15% complete

remission, 9% ESRF at 25yrs and 41% at

15yrs.


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.Rapidly ProgressiveGlomerulonephritis


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Rapidly Progressive Glomerulonephritis

Rapidly progressive

glomerulonephritis (RPGN) is a

disease of the kidney that results ina rapid decrease in the glomerular

filtration rate of at least 50% over

a short period, from a few days to 3months.



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The cause of RPGN is unknown. Agenetic predisposition may exist for thedevelopment of this disease.

Multiple studies have demonstrated thatANCA-(antineutrophil cytoplasmicantibodies) activated neutrophils

attack vascular endothelial cells.ANCA-associated vasculitis.

A viral etiology is possible.


Etiology

R idl P i Gl l h iti


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Pathology

Renal biopsshowA diffuse, proliferative,

necrotizingglomerulonephritis withcrescent formation.

The main pathologicfinding is fibrinoid

necrosis(>90% of biopsyspecimens); extensivecrescent formation ispresent in at least 50% ofglomeruli.



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p y g p

Clinical Manifestations

Symptoms and signs of renal

failure,

pain,haematuria,

systemic symptoms (fever, malaise,myalgia, weight loss).

R idl P i Gl l h iti


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Lab Studies

The most important requirement in the diagnosis ofantineutrophil cytoplasmic antibodies (ANCA) ANCA-associated disease is a high index of suspicion. Rapiddiagnosis is essential for organ preservation. Laboratorystudies include the following:

Routine chemistry: The most common abnormality isan increased serum creatinine level.

Urinalysis with microscopy:

Antinuclear antibody (ANA) titer:

ANCA

Urine and serum protein electrophoresis: Perform this inany middle-aged or elderly person presenting with RPGNto exclude the presence of light-chain disease or overtmultiple myeloma as a cause of the clinical findings.



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Treatment

1-High-dose corticosteroids;

cyclophosphamide plasma

exchange/ renal2-Transplantation.

Prognosis:Poor if initial serum creatinine

>600mol/L.


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Proteinurea

3.5 g/day

(protein: creatinine

ratio >3-3.5)

Generalized

Oedema

Hypoalbuminaeia


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The Nephrotic Syndrome

Is not a disease but a group of signs and

symptoms seen in patients with heavy

proteinuria

presents with oedema

proteinuria usually > 3.5g / 24hrs (>0.05g

/ kg / 24hrs in children)

serum albumin < 30g/l

other features: hyperlipidaemia, and

hypercoaguable state

The Nephrotic Syndrome


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p y

Pathophysiology

proteinuria: due to an increase in glomerular

permeability

hypoalbuminuria: occurs when liver synthesis cannot

keep up with urine losses

oedema mechanism is complex and still in dispute:

primary salt and water retention associated withreduced renal function as well as reduced plasma

oncotic pressure are primary factors (overfill and

underfill)

minimal change disease fits the underfill theory best hyperlipidaemia: increased liver synthesis

hypercoagulation: increased fibrinogen and loss of

antithrombin III


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D M GED Proteinuria


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Primary (idiopathic):

Minimal change disease

Most common cause in children

Membranous Nephropathy

Most common cause in Adults

Focal Segmental Glomerulosclerosis

MembranoProliferative

Glomerulonephritis


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Secondary to:DM(the leading cause of secondary nephrotic syndrome)

SLE

AmyloidosisInfections:Hepatitis B and C, HIV,syphilis, post-streptococcal

Malignancy:

multiple myloma , Hodgkin lymphoma, solid tumorDrugs(NSAIDs, gold, penicillamine ,heavy metals etc).


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Generalized Odema

-The predominant feature

-The face, particularly the

periorbital area, is swollen

in the morning& lower extremitiesand genital area later in the day

-In advanced disease: the whole body

(anasarca) shortness of breathFrothy urine and urine dipstick

proteinuria value of 3+

Symptoms & signs for secondary cause if present


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24-hour urine collection>3,5 g/day (nephrotic-range proteinuria)

Alternative : calculating the total protein-to-creatinine ratio (mg/mg)on a random urine specimen.

The history and physical examination

Systemic diseaseSerologic studies (ANA), complement, hepatitis B and hepatitis Cserologies and the measurement of cryoglobulins ,serum or urine protein

electrophoresis.

Renal biopsyrequired to establish the diagnosis in most of times.


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BUN, creatinine, creatinin clearnce.Na,

K,bicarbonates,chloride

CBC , serum albumin, serum proteins, calcium,

Lipid profile, Coagulation tests

Renal biopsy


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Disease-

spesific

Complication

symptoms


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OedemaLow salt diet

Diuretics

serial measurement of body weight

ProteinuriaACE inhibitors or ARBs

HypoalbuminaemiaHigh protein diet not indicated0.81 g/kg/day

Ref: Up to date online 17.3.


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HyperlipidaemiaRegular Lipid profileStatin if severe long lasting nephrotic syndrome

Control other CVD risk factorstarget blood pressure

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Thromboembolic riskRoutin Prophylactic anticoagulationnot recommend

High index of suspicion for thromboemboli

InfectionsHigh index of suspicion

Antipneumococcal and influenza vaccinations

Ref: Up to date online 17.3.


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y


NEPHROLOGY-II



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.Other Renal Diseases


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Other Renal Diseases

1. 1-Interstitial Nephritis

2. 2-Diabetic Nephropathy

3. 3-Microscopic Vasculitis and SLE

4. 4-Gout and the Kidney

5. 5-Myeloma Kidney


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.1-Interstitial Nephritis


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Causes of interstitial nephritis

Drugs

Infection

Autoimmune

Metabolic

Radiation Neoplastic infiltration

Mechanical


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Drugs and interstitial nephritis

methicillin 17%other penicillins


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Bacterial infection

bacterial infection of the renal parenchyma

causes interstitial nephritis

infection without anatomical abnormalityseldom produces permanent damage

obstruction (stones, prostate etc) in

combination with infection can cause

progressive disease tuberculosis causes extensive destruction from

granulomata, fibrosis and caseation


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Autoimmune

systemic lupus

erythematosus

transplantrejection

deposition of :

calcium salts

uric acid


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Infiltration in neoplastic and other

diseases

lymphoma and leukaemias

myeloma

Bence-Jones protein (light chains frommalignant plasma cell clone) causes interstitial

nephritis, tubular obstruction(cast nephropathy)

and amyloid deposition

called myeloma kidney

sarcoidosis


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mechanical causes of interstitial

nephritis

reflux nephropathy

calculi

ureteric fibrosis

prostatic hypertrophy

urethral stenosis

tumours


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pathophysiolgical changes in

interstitial nephritis

hypertension (50%)

proteinuria (~1-2 g/24hrs)

reduced urinary concentrating ability

salt wasting

renal tubular acidosis


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Diagnosis and Treatment

renal impairment

inactive urine sediment common (cf nephritis)

eosinophils in urine and interstitium in acute

hypersensitivity reactions

renal biopsy

improvement after withdrawal of drugs and toxins

use of corticosteroids (prednisone)

water and and electrolyte

treatment of hypertension


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.2-Diabetic nephropathy


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Diabetic Nephropathy

Pathological lesions:

diffuse glomerular sclerosis

nodular sclerosis (Kimmelstiel -Wilson lesion)

arteriolar hyalinisation

Associated lesions:

Papillary necrosis

Pyelonephritis Bladder dysfunction

Radio contrast renal failure

hyporeninaemic hypoaldosteronism with

hyperkalaemia


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Pathophysiology of Diabetic Nephropathy

renal hypertrophy and hyperfiltration

microalbuminuria (< 100mg/24hrs and negative to

protein test strip-albustix)

hypertension

hyperfiltration and microalbuminuria can be improved

by good diabetic control

microalbuminuria is a predictor of diabetic

nephropathy and mortality in diabetics - it probably

has no predictive value for other renal diseases


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WHO classificationLupus Nephritis Type I no pathology


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Lupus Nephritis Type I no pathology

yp

eV:membranous

Type II : mesangial

TypeIII:fo

cal

proliferative

Ty

peIV:diffu

se

proliferative


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Lupus nephritis

Hematuria and proteinuria

HTN common

Active urine sediment: rbc casts

Decreased C3 and C4

anti-double stranded DNA antibody specific foractive nephritis

Prognosis varies greatly based on initialpathology, usually guarded

Type IV greatest risk of progressing to CKD stage 5

Treatment with steroids, cytoxan


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Systemic Lupus Erythematosus

Diagnosis:

clinical presentation - rash, arthralgia, fever,

tiredness, anaemia etc

hypocomplementaemia - (low C3 and C4)

antinuclear antibodies and anti DNA antibodies

Treatment:

depends on histological severity (WHO class I - V) nearly all get corticosteroids

WHO Class IV usually get corticosteroids and

cyclophosphamide


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.Gout, Uric Acid and Renal

Disease


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Gout, Uric Acid and Renal Disease

uric acid calculi, parenchymal deposits of

uric acid and tubular obstruction with

urate can cause renal damage an elevated plasma uric acid does not in

itself seem to cause renal damage

1/4 of patients with gout get uric acidstones

1/4 of patients with uric acid stones will

have gout


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Acute and Chronic urate nephropathy

acute nephropathy with overproduction of uric acid

and kidney obstruction with uric acid crystals

can occur with treatment of malignant disease with

cytotoxics, heat stroke and status epilepticus

treat with fluids and prophylaxis with allopurinol

role of uric acid in chronic renal failure disputed but

does occur with some familial disorders

association between hyperuricaemia, hypertensionvascular disease, hyperlipidaemia and diabetes


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.Amyloidosis and MyelomaKidney


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Amyloidosis and Myeloma Kidney

amyloid represents a family of proteins which

polymerize to produce the beta pleated sheet of

amyloid and deposit in tissues

AL amyloid (primary amyloid) made from

light chains associated with plasma cell

disorders, mostly overt myeloma

AA amyloid (secondary amyloid) is made fromA protein and is an acute phase reactant

associated with chronic inflammatory diseases

like rheumatoid arthritis and bronchiectasis


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NEPHROLOGY-III



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.Acute Renal Failure


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Acute renal failure -ARF

Deterioration of renalfunction over a period of hours to days,resulting in

the failureof the kidney to excrete nitrogenouswaste products and

to maintainfluid and electrolyte homeostasis ARF Rapid deterioration of renal function

(increase of creatinine of >0.5 mg/dl in


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Hilton, R. BMJ 2006;333:786-790


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Pre-renal

Volume depletion Renal losses (diuretics, polyuria)

GI losses (vomiting, diarrhea)

Cutaneous losses (burns, Stevens-Johnson syndrome)

Hemorrhage Pancreatitis

Decreased cardiac output Heart failure

Pulmonary embolus

Acute myocardial infarction Severe valvular heart disease

Abdominal compartment syndrome (tense ascites)

Renal


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Glomerular Antiglomerular basement membrane (GBM) disease (Goodpasture

syndrome)

Antineutrophil cytoplasmic antibody-associatedglomerulonephritis (ANCA-associated GN) (Wegenergranulomatosis, Churg-Strauss syndrome, microscopic polyangiitis)

Immune complex GN (lupus, postinfectious, cryoglobulinemia,

primary membranoproliferative glomerulonephritis) Tubular

Ischemi

Totoxic

Heme pigment (rhabdomyolysis, intravascular hemolysis)

Crystals (tumor lysis syndrome, seizures, ethylene glycolpoisoning, megadose vitamin C, acyclovir, indinavir,methotrexate)

Drugs (aminoglycosides, lithium, amphotericin B,pentamidine, cisplatin, ifosfamide, radiocontrast agents)


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Post-renal

Ureteric obstruction

Stone disease,

Tumor,

Fibrosis,

Ligation during pelvic surgery

Bladder neck obstruction

Benign prostatic hypertrophy [BPH]

Cancer of the prostate

Neurogenic bladder

Drugs(Tricyclic antidepressants, ganglion blockers, Bladder tumor,

Stone disease, hemorrhage/clot)

Urethral obstruction (strictures, tumor)


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Clinical feature-1

Signs and symptoms resulting from loss of

kidney function:

decreased or no urine output, flank pain,edema, hypertension, or discolored urine

Asymptomatic

elevations in the plasma creatinine

abnormalities on urinalysis


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Clinical feature-2

Symptoms and/or signs of renal failure: weakness and

easy fatiguability (from anemia),

anorexia, vomiting, mental status changes or

Seizures

edema

Systemic symptoms and findings: fever

arthralgias,

pulmonary lesions

Acute Renal Failure


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Acute Renal Failure

Diagnosis Blood urea nitrogen and serum creatinine

CBC, peripheral smear, and serology

Urinalysis Urine electrolytes

U/S kidneys

Serology:ANA,ANCA, Anti DNA, HBV, HCV, AntiGBM, cryoglobulin, CK, urinary Myoglobulin

Acute Renal Failure


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Acute Renal Failure

Diagnosis Urinalysis

Unremarkable in pre and post renal causes

Differentiates ATN vs. AIN. vs. AGN Muddy brown casts in ATN

WBC casts in AIN

RBC casts in AGN

Hansel stain for Eosinophils

Acute Renal Failure


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Acute Renal Failure

Diagnosis Laboratory Evaluation:

Scr, More reliable marker of GFR

Falsely elevated with Septra, Cimetidine small change reflects large change in GFR

BUN,generally follows Scr increase

Elevation may be independent of GFR

Steroids, GIB, Catabolic state, hypovolemia

BUN/Cr helpful in classifying cause of ARF

ratio> 20:1 suggests prerenal cause

Treatment of

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acute renal failure

Optimization of hemodynamic and

volume status

Avoidance of further renal insults Optimization of nutrition

If necessary, institution of renal

replacement therapy The function has to be temporarilyreplaced by dialysis

Indication for dialysis


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Symptoms of uremia (

encephalopathy,)

Uremic pericarditis Refractory volume over load

Refractory hyperkalemia

Refractory metabolic acidosis


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.Chronic Renal Failure

Definitions


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Definitions

Chronic Renal Failure Results form gradual, progressive loss of renalfunction

Occasionally results from rapid progression of

acute renal failure Symptoms occur when 75% of function is lost

but considered cohrnic if 90-95% loss offunction

Dialysis is necessary D/T accumulation oruremic toxins, which produce changes in majororgans

S bj ti t


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Subjective symptoms

Chronic Renal Failure Subjective symptoms are relatively same as

acute

Objective symptoms

Renal Hyponaturmia

Dry mouth

Poor skin turgor

Confusion, salt overload, accumulation of K withmuscle weakness

Fluid overload and metabolic acidosis

Proteinuria, glycosuria

Urine = RBCs, WBCs, and casts

Ch i R l F il


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Chronic Renal Failure

Objective symptoms

Cardiovascular Hypertension

Arrythmias

Pericardial effusion

CHF

Peripheral edema

Neurological Burning, pain, and

itching, parestnesia Motor nerve dysfunction

Muscle cramping

Shortened memory span

Apathy

Drowsy, confused,seizures, coma, EEG

changes

Ch i R l F il


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Objective symptoms

GI

Stomatitis

Ulcers

Pancreatitis

Uremic fetor

Vomiting consitpation

Respiratory

^ chance of

infection

Pulmonary edema

Pleural friction

rub and effusion

Dyspnea

Kussmauls

respirations from

acidosis

Ch i R l F il


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Objective symptoms

Endocrine

Stunted growth in

children Amenorrhea

Male impotence

^ aldosterone secretion

Impaired glucose levels

R/T impaired CHOmetabolism

Thyroid and parathyroid

abnormalities

Hemopoietic

Anemia

Decrease in RBCsurvival time

Blood loss from dialysis

and GI bleed

Platelet deficits

Bleeding and clotting

disorderspurpura and

hemorrhage from body

orifices , ecchymoses

Ch i R l F il


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Objective symptoms

Skeletal

Muscle and bone pain

Bone demineralization

Pathological fractures

Blood vessel

calcifications in

myocardium, joints,

eyes, and brain

Skin

Yellow-bronze skin

with pallor Puritus

Purpura

Uremic frost

Thin, brittle nails

Dry, brittle hair, and

may have color

changes and alopecia



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Lab findings

BUNindicator of glomerular filtration rate and isaffected by the breakdown of protein. Normal is 10-20mg/dL. When reaches 70 = dialysis

Serum creatininewaste product of skeletal musclebreakdown and is a better indicator of kidneyfunction. Normal is 0.5-1.5 mg/dL. When reaches 10x normal, it is time for dialysis

Creatinine clearance is best determent of kidneyfunction. Must be a 12-24 hour urine collection.

Normal is > 100 ml/min K+ -

Hypocalcemia = tetany

Ch i R l F il


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Other abnormal findings

Metabolic acidosis

Fluid imbalanceInsulin resistance

Anemia

Immunoligical problems

Chronic Renal FailureM di l t t t


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Medical treatment

IV glucose and insulin

Na bicarb, Ca, Vit D, phosphate binders

Fluid restriction, diuretics Iron supplements, blood, erythropoietin

High carbs, low protein

Dialysis - After all other methods have failed


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Peritoneal dialysis Semipermeable

membrane

Catheter inserted through

abdominal wall intoperitoneal cavity

Cost less

Fewer restrictions

Can be done at home

Risk of peritonitis 3 phasesinflow, dwell

and outflow

Automated peritoneal

dialysis

Done at home at night

Maybe 6-7 times /week CAPD

Continous ambulatory

peritoneal dialysis

Done as outpatient

Usually 4 X/d



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Transplant

Must find donor

Waiting period long Good survival rate1 year 95-97%

Must take immunosuppressants for life

Rejection

Watch for fever, elevated B/P, and pain over site

of new kidney

Transplant Meds


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Transplant Meds

Patients have decreased resistance to infection

Corticosteroidsanti-inflammarory

Deltosone

Medrol Solu-Medrol

Cytotoxicinhibit T and B lymphocytes

Imuran

Cytoxan

Cellcept

T-cell depressors - Cyclosporin


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C M di i I t


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NEPHROLOGY-IV



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.RENAL TUMOURS


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.

YSTIC DISE SES OFTHE KIDNEY

CYSTIC DISE SES OF


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THE KIDNEY Fluid filled spaces within the kidney

May involve cortex or medulla or both

May be unilateral or bilateral May be unilocular or multilocular

May be congenital or acquired

May be sporadic or geneticallydetermined

Clinical significance may be trivial or

CLASSIFICATIONS OF


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RENAL CYSTIC DISEASES

Polycystic kidney diseases:

1. Autosomal recessive (ARPKD)

classic infantile polycystic diseasewith congenital hepatic fibrosis

2. Autosomal dominant (ADPKD)

Simple renal cysts

Acquired renal cystic disease

RENAL CYSTIC DISEASES


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Enlarged but normally shaped pelvi-calyceal

system Normal reniform shape complete with fetal

lobation & normal sized (undilated) ureter

Normal glomeruli and tubules

Normal interstitium and no dysplasia

Congenital hepatic fibrosis is almost always

present

Normal numbers of nephrons, no interstitialfibrosis and no dysplasia


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RENAL CYSTIC DISEASESP th l i l F t


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Pathological Features

Bilaterally enlarged kidneys (up to 4000 gms) Diffuse cystic (1-2% cystic nephrons) change

with uninvolved intervening parenchyma

Varying sized, numerous to innumerable

generally spherical unilocular cysts, distributedin cortex and medulla obscuring normalreniform shape and corticomedullary junction,containing yellowish to turbid to brown to black

colored fluid Distorted pelvi-calyceal system

Cysts arising from any part of nephron orcollecting duct


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Simple Renal Cysts


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Extremely common as age advances Incompletely understood pathogenesis

Commonly associated with scarred

kidneysAsymptomatic with normal renal function

May be

solitary/multiple/unilateral/bilateral

Generally unilocular, round to oval of

varying sizes


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Adult polycystic kidney disease


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Renal cancer

.

Renal cancer


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In infants and children :Nephroblastoma ( Wilms

tumour )In adults :

Renal cell carcinoma

Renal cell adenoma

Renal oncocytoma


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NEPHROBLASTOMA


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prognosis and treatment

Depends upon :

stage, age and histology

Surgery with chemotherapy for :stage I & II with favorable histology

surgery with chemotherapy and

radiotherapy for higher stages andunfavorable histology

RENAL CELL CARCINOMA


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Hypernephroma / Grawitzstumour

seems to be arising from maturerenal tubules

RENAL CELL CARCINOMACli i l F t & Di i


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Clinical Features & Diagnosis

classic triad :

hematuria, flank pain and abdominal

mass may be clinically occult, 30% presents

with metastatic lesion

Polycythemia due to erythropoietin constitutional symptoms

imaging techniques - useful


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RENAL CELL

CARCINOMA


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CARCINOMA

prognosis Influenced by multiple factors :tumour size

infiltrative marginshistological type

tumour stage - most important

Can be expressed in terms of histologicaltypes


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Renal cell carcinoma


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Bladder Carcinoma


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Derived from transitional epithelium

Present with painless hematuria

Prognosis depends on grade and depth of invasion

Overall 5y survival = 50%


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.DIALYSIS

Dialysis


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Definition Artificial process that partially replaces renal

function

Removes waste products from blood bydiffusion (toxin clearance)

Removes excess water by ultrafiltration

(maintenance of fluid balance) Wastes and water pass into a special liquid

dialysis fluid or dialysate

Types


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yp

Haemodialysis (HD)

Peritoneal Dialysis (PD)

They work on similar principles: Movementof solute or water across a semipermeable

membrane (dialysis membrane)

Diffusion


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Movement of solute

Across semipermeable membrane

From region of high concentration to one oflow concentration

Ultrafiltration


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Made possible by osmosis

Movement of water

Across semipermeable membrane From low osmolality to high osmolality

Osmolalitynumber of osmotically active

particles in a unit (litre) of solvent

Haemodialysis

Dialysis process occurs outside the body in a


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Dialysis process occurs outside the body in a

machine The dialysis membrane is an artificial one:

Dialyser

The dialyser removes the excess fluid andwastes from the blood and returns the filteredblood to the body

Haemodialysis needs to be performed threetimes a week

Each session lasts 3-6 hrs


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AV Fistula Access

Matures in about 6 weeks


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Ensure good working order Avoid tight clothing or wrist watch on fistula arm

Assess fistula daily; notify immediately if not working

Avoid BP cuff on fistula arm Avoid blood sampling on fistula arm (except daily

HD Rx)

Avoid sleeping on fistula arm

Grafts (synthetic) may be used to create an AV fistula


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AV Fistula


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AV Fistula


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Vascular Access Catheter


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Hemodialysis


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3-4 times a week

Takes 2-4 hours

Machine filtersblood and

returns it to

body

Problems with HD Rapid changes in BP fainting, vomiting, cramps, chest pain, irritability, fatigue, temporary loss

of vision

Fl id l d


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Fluid overload

esp in between sessions Fluid restrictions

more stringent with HD than PD

Hyperkalaemia

esp in between sessions

Problems with access poor quality, blockage etc. Infection (vascular access catheters)

Bleeding

from the fistula during or after dialysis Infections

during sessions; exit site infections; blood-borne viruses e.g. Hepatitis,HIV

Peritoneal Dialysis (PD)

U l b ( i ) f


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Uses natural membrane (peritoneum) for

dialysis

Access is by PD catheter, a soft plastic tube

Catheter and dialysis fluid may be hidden

under clothing

Suitability

Excludes patients with prior peritoneal scarring e.g.

peritonitis, laparotomy

Excludes patients unable to care for self

Peritoneal Dialysis

.


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Principles of Peritoneal Dialysis(PD)Standard dialysis solution contains:

Na+ 132 mEq/l


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Na+ 132 mEq/l

Cl- 96 -102 mEq/l

Ca2+ 2.53.5 mEq/l

Mg2+ 0.5 -1.5 mEq/l

Dialysis solution buffer: Sodium lactate

Pure HCo3-

HCo3- /Lactate combinations

Lactate is absorbed and converted to HCo3-by

the liver

Dextrose solution strengths: 1.5%, 2.5%, 4.25%

Types


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Continuous Ambulatory Peritoneal Dialysis

(CAPD)

Automated peritoneal Dialysis (APD) Continuous cyclical

Intermittent

Continuous Ambulatory Peritoneal Dialysis

(CAPD)


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CONTROLLING YOURDIET


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Foods to control are those containing: Protein

Potassium

Sodium

Phosphorous

Fluid

FLUIDS


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Healthy kidneys remove fluids as urine

Check for fluid and sodium retention

Need to restrict fluid intake

VITAMINS


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Folic acid

Iron supplements

Do not take OTCs without consulting thedoctor.

MANAGING YOUR DIET


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INDICATORS OF GOOD CONTROL:

Weight loss or gain

Blood pressure

Swelling of hands and feet

Blood samples

Plasmapheresis:

plasma exchange and immunoadsorption


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An adult donor kidney transplanted to the left iliac

fossa of an adult recipient


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.


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.Kidney Stones


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4. CystineCystinuria is an herditary disease which is more common

in infants and children. Only a small percentage of patients with

Cystinuria form stones.

5. Drug induced stones

In rare cases, the long term use of magnesium trisilicate in

the treatment of peptic ulcer has produced radio opaque silicon

stones.

LOC TION OF STONES IN KIDNEY


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.

CLINIC L FE TURESSymptoms- Symptom wise cases can be divided into 4 groups :-

1. Quiescent calculus A few stones, particularly the phosphate


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Q , p y p p

stones, may lie dormant for quite a long period.These stone are also discovered due to symptoms of Urinary

Infection

2. Pain- Plain is the leading symptom of renal calculus in majority of

cases (80%). Three types of pain .

a) Fixed renal pain

b) Ureteric colic

c)Referred pain

3. Hydronephrosis

4. Occasionally haematuriais the leading and only symptom.

(iii) Swelling- When there isHydronephrosis orpyonephrosisassociated with renal calculus, a swelling may be felt

in the flank.

The characteristic of a renal swelling are :-


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g

(a) Oval or reniform in shape

(b) Swelling is almost fixed and cannot be moved.

(c) A kidney lump is ballot able.

3.Radiography

A) STRAIGHT X-RAY-Before taking straight X-ray for KUB region (both

kidneys, ureters and bladder), the bowels must be made empty by giving laxative.


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B) Excretory Urogram

4 Ultrasonography

Helpful to distinguish between opaque and non-opaque stones. It is also of

value in locating the stones for treatment with extra corporeal shock wave therapy.

5 Computed topography

Particularly helpful in the diagnosis of non-opaque stones.

6 Renal Scan

7 I nstrumental examination:- Cystoscopy

8 Examination of the stone

MANAGEMENT OF


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NEPHROLITHIASIS

.

ASYMPTOMATIC CALCULI


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TREATMENT

Solitary kidneyOccupation (pilot, business traveler

Simultaneous contralateral treatment

Its difficult to make an asymptomatic patientfeel any better !

STONE MANAGEMENT


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OPTIONS

Open surgery

Percutaneous

nephrolithotomy

Ureteroscopy

Shock wave lithotripsy

Medical therapy


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SHOCK WAVE LITHOTRIPSY.


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SHOCK WAVE LITHOTRIPSYSTONE FRAGMENTATION


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SHOCK WAVELITHOTRIPSY


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INDICATIONS

Surgical stone

No obstruction

Reasonable chanceof expeditious removal



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RELATIVE CONTAINDICATIONS

Large stones

Calcium oxalate > 20 mmStruvite > 30

mm

Cystine stones

Distal obstruction

Poorly informed patients

SHOCK WAVE LITHOTRIPSY


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CLINICAL SIDE-EFFECTS

Hematuria

Pain

Obstruction

(Steinstrasse)



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IDEAL CANDIDATES

Small stone (< 1.5 cm)

Mid or upper pole location

Normal renal anatomy

No distal obstruction

SHOCK WAVE


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LITHOTRIPSY

LIMITATIONS

Completeness of stone fragmentation

Completeness of fragment elimination

STONE MANAGEMENTPERCUTANEOUS NEPHROLITHOTOMY


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SURGICAL STONEMANAGEMENT


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CURRENT ROLE OF PNL



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STAY OUT OF TROUBLE

Pre-op KUB Pre-op IVP

URETERAL CALCULI


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URETERAL CALCULI


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TREATMENT OPTIONS

Observation

Shock wave lithotripsyUreteroscopy

Blind basket extraction

Percutaneous approach

Open surgery


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.


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.FINAL


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ACUTE AND CHRONIC

INTERSTITIAL NEPHRITIS

.

Morphology of the interstitium


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Fibrosis develops after infiltration by

mononuclear cells (lymphocytes) which is

accompanied by deposition of fibronectin,

collagen type I, III, VI and IV.

There is a physiological balance between

ongoing matrix formation and - degradation.

Morphology of the interstitium


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Composed of a loosely organized matrix

consisting of the collagen types I and III,

proteoglycans containing the interstitial

cells:

matrix producing fibroblasts

macrophages

dendritic reticulum cells

endothelial cells

Importance of interstitial cells


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Interstitial fibroblasts:

Fibrogenesis

Production of erythropoietine (they lose this functionduring the process of fibrogenesis)

Can transform into myofibroblasts (expression of SMA)

Changes in the interstitial area play an important negativepredictive value on the long term follow up of the primarykidney disease. Important and determining factors are

interstitial volume (=fibrosis) and inflammation

Interferences with theinterstitium: broad


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spectrum Infection: direct (BK virus, TBC, acute pyelonephritis),

indirect( Streptococci)

Immunologic

Allergic: druginduced

Auto-immune: Sjgren syndrome

Alloimmune: acute cellular allograft rejection

Unknown: IgG4- associated acute interstitial nephritis

Toxic: Pb poisoning, cadmium poisoning, Balkan endemicnephropathy

Metabolic: oxalosis secondary to malabsorbtion , gout

Obstruction: ureteral- pelvic junction stenosis:

Radiation: radiation interstitial nephritis

Idiopathic: sarcoidosis

Different entities of interstitial disease


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Acute interstitial nephritis

Chronic interstitial nephritis

Acute pyelonephritis

Chronic pyelonephritis (reflux related)

Xanthogranulomatous pyelonephritis

Malakoplakie

Myeloma kidney

IgG4 interstitial nephritis

Lead induced interstitial nephritis

Urate nephropathy

TX related Polyoma induced interstitial nephritis

Balkan interstitial nephritis

Acute interstitial nephritis


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Most common etiologies are:

a) those related to the use of medications: 85%

b) those related to infectious agents: 10%

c) those associated to systemic disease or

glomerular diseases: 1%

d) idiopathic disease: 4%

Acute interstitial nephritis:

drugs


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Etiology: AB (penicillins and cephalosporins, methicillin),diuretics, NSAIDs, chinese herbs, lithium

Pathogenesis:

T cell mediated allergic - immune reaction on drug or drug-self

protein conjugate (hapten) later followed by accumulation oflymphocytes, plasmocytes and histiocytes

Histology: Early signs: oedema, lymphocytes focally

Later: eosinophils, lymphocytes, plasmocytes and histiocytes with

granuloma formation(with giant cells) in 30 %, especially after AB Tubulitis (distal tubules): with breaks of TBM, necrosis of tubular

cells and atrophy and loss of tubules.

Tamm Horsfall may find its way to the interstitium (DDobstruction of nephron).

Acute drug induced interstitial

nephritis

Oedema and focal inflammation


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Granuloma

EOS


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Granuloma

Acute drug induced interstitial

nephritis


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Normally are the glomeruli not afflicted.

One exception: use of NSAIDs: can

combine ARF with Nephrotic Syndrome

(effect of cell- mediated lymphokine

directed reaction) inducing Minimal

Lesions (effacement of foot processes of

podocytes)

Acute interstitial nephritis:

clinics


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Acute Renal Failure andreduced glomerularfiltration rate:

- depends on the severity of

inflammation- interstitial oedema causes

elevated intratubular pressure

- intratubular obstruction throughintra luminal cells

- tubular backleak- vasoconstriction

- tubuloglomerular feedback

Outcome of druginduced

interstitial nephritis


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Recovery?

Drug withdrawal: 60-

90% in 1 to 12 mths Irreversible with

analgesics, NSAIDs,

longterm use

Adverse prognostic

features

Marked interstitial

inflammation Granuloma (50%

irreversible)

Tubular atrophy

Fibrosis

Acute interstitial infectious

nephritis


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Infectious:direct invasion or remote infectionsbacteria ( hemolytic streptococci), parasites(Leishmania) and viruses (EBV, measles)

Pathogenesis: immunological hypersensitivityreaction to the infectious agent, effect ofchemokines produced by the kidney in response

Histology: Early signs: invasion by lymphocytes, eosinophils around the veins

In casu there is tubular destruction: histiocytes accumulate

Tubulitis with disappearance of the brush border in proximaltubules

ACUTE INTERSTITIAL INFECTIOUS NEPHRITIS


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Chronic interstitial nephritis


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Papillary sclerosis

CIN


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Interstitium in transplants


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Calcineurin inhibitors:

Heart, liver, pancreas, kidney transplants indifferent doses

Different levels of interstitial damage Most structural nephrotoxic effects in arterioles

and glomeruli are manifestations of ThromboticMicroAngiopathy(TMA) with different patterns

of severity. The interstitial fibrosis has anuncertain pathogenesis but is probably vascular.

Toxicity of calcineurin

inhibitors


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Cellular rejection in kidney Tx


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Histology:

Very early: eosinophils

Followed by T lymphocytes

Later: Plasmocytes IgG+ if IgM+ : be aware of

polyoma infection

In peritubular capillaries (PTC):

lymphocytes++

Cellular rejection


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Tubulitis

CD3



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Etiology: ascending infection from the pyelon

Pathogenesis: microbial release of degradative

enzymes and toxic molecules, direct contact or

penetration of the host cell by the infectious agentand the inflammatory response mediated by

antibodies, T cells

Histology:

Tubules are damaged by neutrophils (Congored)



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Chronic pyelonephritis

E i l fl


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Etiology: reflux

Histology:

- wedge shaped interstitial fibrosis(follows the

traject of the papillae and ascending tubules)accompanied by tubular atrophy, vascularatheromatosis, glomerular sclerosis, inflammation

- outside the wedges: normal parenchyma but

with secondary changes in the glomeruli:glomerular hypertrophy, FSGS



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Tubular disease

A t t b l d


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Acute tubular damage:

Ischemia: vasoconstriction with endothelial activation

will determinate the extent of the tubular cell loss:

cellular, geographic, focal

Toxins:

Myoglobinuria

Heavy metal exposure (Pb, Cd)

Oxalate crystal deposits: ethylene glycol toxicity

Calcineurin inhibitors: megamitochondria, isometricvacuolisation

Tubular damage


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URETERAL CALCULI


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Stone-free is not everything !!

PARAMETERS FOR COMPARISON

URETERAL CALCULI


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Effectiveness

Morbidity

Convalescence

Cost

PARAMETERS FOR COMPARISON


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DISTAL URETERAL CALCULI


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URS is 10 - 18% more effective than SWL(depending on type of SWL unit)

Morbidity / convalescence reduced with SWL

Need for stents 40-60% less with SWL

Cost issues not addressed in monotherapy studies

COMPARISON OFMONOTHERAPY STUDIES


OVERVIEW OF HISTORICAL


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SWL URSEffectiveness Slightly better

Morbidity Less

Hospitalization LessCost Slightly less

OVERVIEW OF HISTORICALCONTROL STUDIES



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80 patients randomized to receive SWL or URS 40patients had stones > 5 mm40 patients had stones < 5 mm

SWL performed on Dornier MFL 5000

URS performed with 6.5F or 9.5F semi-rigidureteroscopes (basket vs. pneumatic lithotripsy)

PROSPECTIVE, RANDOMIZED TRIAL

Peschel & Bartsch, 1999


PROSPECTIVE RANDOMIZED TRIAL


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URS SWL

OR time (min) 19 63Fluoro time (min) 0.8 5.1

Stone-free (days) 0.2 10.8

Stent (days) 7.2 0Re-treatmentrate 0 15%

PROSPECTIVE, RANDOMIZED TRIALSTONES < 5 MM

Peschel & Bartsch, 1999

***

**

SWL OF DISTALURETERAL CALCULI


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Initial animal studies suggest ovarian traumaImpaired fertilityMutagenesis

Subsequent animal investigations demonstrate no

impact on fertility or offspringMice Rats Rabbits

ADVERSE EFFECTS TOFEMALE REPRODUCTIVE TRACT?

SWL OF DISTALURETERAL CALCULI


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Analyzed Rx data and radiation exposurein 84 women of reproductive age

7 children born to 6 patients with no

malformations or chromosomalanomalies

Miscarriages in 3 patients (but occurredat least 1 year after SWL)

ADVERSE EFFECTS TOFEMALE REPRODUCTIVE TRACT?

Viewig & Miller, 199

URETEROSCOPY


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URETERAL CALCULI

FLEXIBLE URETEROSCOPY


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FLEXIBLE URETEROSCOPY

ANTEGRADE MANIPULATION OFURETERAL CALCULI


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Large stone burden

Body habitus

Urinary diversionTransplant kidney

INDICATIONS

URETERAL CALCULI

PERCUTANEOUS APPROACH


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PERCUTANEOUS APPROACH

URETERAL STONEMANAGEMENT

IN SITU SWL


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AdvantagesMinimal anesthesia requirements

Non-invasive procedureNo stenting/less complicationsSimilar approach for all ureteralcalculi

DisadvantagesLower success rate than URSHigher re-treatment rate

IN SITU SWL

URETERAL STONEMANAGEMENT

URETEROSCOPY


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URETEROSCOPYAdvantages

Highest success rate

Definitive Rx - No waiting for stonepassage

Disadvantages

More invasive than SWLHigher complication rateRequires greater technical expertise

URETERAL CALCULI: CURRENTOPTIONS

PROX AND MID URETERAL STONES


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PROX AND MID URETERAL STONES

Approach Invasive Stent S-F Rate Re-

RxRate

URS +++ 100% 75-90% 10-15%

Push/Smash ++ Rarely 92% 9%

SWL + Stent + 100% 75-80% 20-25%

*

Defined as complete stone removal with single procedure

URETERAL CALCULI: CURRENTOPTIONS

DISTAL URETERAL STONES


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DISTAL URETERAL STONES

Approach Invasive Stent S-F Rate Re-

RxRate

URS +++ 100% 98-100% 0-2%

Push/Smash ++ Rarely 92% 9%

SWL + Stent + 100% 75-80% 20-25%

*

Defined as complete stone removal with single procedure


CHANGING TREATMENT


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CHANGING TREATMENTPHILOSOPHIES

1980s 1990s 2000s20

10s

Shock wave lithotripsy 95% 85% 75% ???

Endoscopic procedures 5% 15% 25% ???

Open stone surgery < 1% < 1% < 1% 0

NEPHROLITHIASIS

NATURAL HISTORY & RISK FACTORS


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Peak incidence age 30 - 60

Gender (Male : Female) 3 : 1

Family history 3 - fold risk

Body size risk with weight

Recurrence after first stone:Year 1 10 - 15%Year 5 50 - 60%Year 10 70 - 80%

NATURAL HISTORY & RISK FACTORS


RECURRENT STONE


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RECURRENT STONEFORMATION One Year Two Years

Post SWL Post SWL

Stone FreeNew stones 8% 10%

Residual StonesStone growth 22% 21%

Lingeman, et al, 1989


EFFECT ON STONE RISK


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EFFECT ON STONE RISKFACTORS

Urine Values Pre- 3 Mo Post-(mg/day) Lithotripsy Lithotripsy

Calcium 254 261Uric Acid 552 548

Citrate 249 257

Oxalate 42 41

Brown, et al, 1989

MEDICAL MANAGEMENT OFNEPHROLITHIASIS

PROGRESS


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PROGRESSElucidation

Urinary environment conducive to stone formation

DiagnosisDetection of underlying physiologic abnormalities

Medical TherapyDevelopment of new treatment strategies

STONE FORMATION


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Concentration / solubility of stone-forming

salts

Promoters of crystallization and aggregation

Inhibitors of crystallization and aggregation

MAJOR FORCES

DIETARY CALCIUM


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Early recommendations suggest that low calcium diet

will decrease urinary Ca++excretion, thereby reducingrisk of stone formation

Potential risk factors involving low calcium diet:

Reduced bone mass

Increased urinary oxalate

IMPACT OF LOW CALCIUM DIET

DIETARY CALCIUM

RECOMMENDATIONS


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Moderate calcium restriction in patients with

AH

Limit dietary intake of oxalate

Spinach, tea, chocolate, nutsLimit dietary sodium intake

RECOMMENDATIONS

CALCIUM SUPPLEMENTS


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Calciuric response to calcium supplementation

Depends on duration of treatment and patient

population

PHYSIOLOGICAL EVIDENCE

CALCIUM SUPPLEMENTS

RECOMMENDATIONS:


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Give HCTZ during initial three months to preventhypercalciuria, then discontinue for one month

If urinary calcium up at 4 months, re-start HCTZ

Alternative: Significantly increase fluid intake for

first three months and then check 24-hour urinarycalcium

RECOMMENDATIONS:PREMENOPAUSAL WOMEN

Henoch Schnlein Purupura


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Answer 1.

ReninAngiotensin II- ACE- ADHAldosterone


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That is not correct

Please try again

Peritoneal Dialysis

Is performed as an

intracorporeal (inside thebody) therapy making use of


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p (body) therapy making use ofthe peritoneal membrane.

Is the process of cleaning theblood by using the lining of

the peritoneal cavity(peritoneum) as a filtertheperitoneum acts as adialyzing membrane,permitting wastes from the

body to cross it and emptyinto the instilled dialysatefluid .

Is a type of dialysis usuallydone by the patient at home.


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Hemodialysis

3-4 times a week


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Takes 2-4 hours

Machine filters

blood and

returns it to

body


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Documents

2014 Curs Nefrologie-De Prezentat 4-Ian 2014