Nephrolithiasis, Urinary Tract Obstruction, Vascular Injury to the Kidneys

NephrolithiasisNephrolithiasis

Vimar A. Luz, MD, FPCP, DPSNCenter for Renal Diseases

St. Luke’s Medical Center

Most common urological problems

Most common urological problems13% in men, 7% in women, increasing

in the industrialized world

in the industrialized worldPathogenesis

Pathogenesis

1. Breakdown of balance between solubility and precipitation of salts

Pathogenesis

balanced during adaptation to diet, climate and activity, and also mechanisms of kidneys in inhibiting

crystallization

Pathogenesis

2. Supersaturation

Pathogenesis 1. Breakdown of balance between solubility

and precipitation of salts 2. Supersaturation Metastably supersaturated Upper Limit of Metastability Excessive Supersaturation

Pathogenesis 1. Breakdown of balance between

solubility and precipitation of salts 2. Supersaturation 3. Crystallization

Pathogenesis 1. Breakdown of balance between solubility and

precipitation of salts 2. Supersaturation 3. Crystallization Heterogenous Nucleation (crystals and debris as template for

stone formation) Aggregation as plaques (Randall’s plaques) Oxalate exposure then crystal formation

in the industrialized worldPathogenesisDiagnosis

Diagnosis

1. S/Sx: flank, lower abdominal, gross or micro hematuria

2. CT scan

3. Ultrasound not as sensitive as CT

4. Abdominal Xrays

in the industrialized worldPathogenesisDiagnosis

Types of stones

Types of Stones

Types of Stones 1. Calcium stones

- Ca oxalate and Ca phosphate stones 75 to 85% and admixed in the same stone

- M>F, 3rd to 4th decade

- once a stone former always a stone former ( 1 per 2 to 5 years)

- Idiopathic Calciuria

NephrolithiasisNephrolithiasis Idiopathic Calciuria

- most common abnormality found in nephrolithiasis

- familial, can be poly and monogenic

- hypercalciuria, nephrocalcinosis and progressive kidney failure

NephrolithiasisNephrolithiasis Idiopathic Calciuria - most common abnormality found in nephrolithiasis - familial, can be poly and monogenic - hypercalciuria, nephrocalcinosis and progressive

kidney failure - Dx hypercalciuria w/o hyperCa and the absence of

ther disorders affecting Ca/P metabolism

NephrolithiasisNephrolithiasis Idiopathic Calciuria - most common abnormality found in nephrolithiasis - familial, can be poly and monogenic - hypercalciuria, nephrocalcinosis and progressive

kidney failure - Dx hypercalciuria w/o hyperCa and the absence of ther

disorders affecting Ca/P metabolism - Absorptive and Renal

NephrolithiasisNephrolithiasis Idiopathic Calciuria - most common abnormality found in nephrolithiasis - familial, can be poly and monogenic - hypercalciuria, nephrocalcinosis and progressive kidney

failure - Dx hypercalciuria w/o hyperCa and the absence of ther

disorders affecting Ca/P metabolism - Absorptive and Renal - Pathogenesis: Vit D overactivity

NephrolithiasisNephrolithiasis Idiopathic Calciuria - most common abnormality found in nephrolithiasis - familial, can be poly and monogenic - hypercalciuria, nephrocalcinosis and progressive kidney failure - Dx hypercalciuria w/o hyperCa and the absence of ther

disorders affecting Ca/P metabolism - Absorptive and Renal - Pathogenesis: Vit D overactivity - Treatment:

NephrolithiasisNephrolithiasis Treatment: 1. Low Ca diet (?) to decrease hypocalciuria

- more stone recurrence vs those treated w/ normal Ca diet, low salt, water intake

NephrolithiasisNephrolithiasis Treatment: 1. Low Ca diet (?) to decrease hypocalciuria

- more stone recurrence vs those treated w/ normal Ca diet, low salt, water intake

2. Low Na, low protein

NephrolithiasisNephrolithiasis Treatment: 1. Low Ca diet (?) to decrease hypocalciuria - more stone recurrence vs those treated w/ normal

Ca diet, low salt, water intake 2. Low Na, low protein 3. Thiazides lowers urinary Ca esp low NaCl intake 4. Citrate supplementation (Acalka)

NephrolithiasisNephrolithiasis Treatment: 1. Low Ca diet (?) to decrease hypocalciuria - more stone recurrence vs those treated w/ normal Ca diet, low salt,

water intake 2. Low Na, low protein 3. Thiazides lowers urinary Ca esp w/ low NaCl intake 4. Citrate supplementation (Acalka) 5. 20% of Calcium oxalate stone formers are hyperuricosuric, low purine

diet (UA salts outs Ca)

NephrolithiasisNephrolithiasis Treatment: 1. Low Ca diet (?) to decrease hypocalciuria - more stone recurrence vs those treated w/ normal Ca diet, low salt, water

intake 2. Low Na, low protein 3. Thiazides lowers urinary Ca esp w/ low NaCl intake 4. Citrate supplementation (Acalka) 5. 20% of Calcium oxalate stone formers are hyperuricosuric, low purine diet (UA

salts outs Ca) 6. If Primary Hyperpara, dx and parathyroidectomy

NephrolithiasisNephrolithiasis Treatment: 1. Low Ca diet (?) to decrease hypocalciuria - more stone recurrence vs those treated w/ normal Ca diet, low salt, water intake 2. Low Na, low protein 3. Thiazides lowers urinary Ca esp w/low NaCl intake 4. Citrate supplementation (Acalka) 5. 20% of Calcium oxalate stone formers are hyperuricosuric, low purine diet (UA

salts outs Ca) 6. If Primary Hyperpara, dx and parathyroidectomy 7. Treat if Type 1 RTA as etiology of stone formation

2. Uric acid stones

Uric acid stones

- Pathogenesis: increase urine acidity plus hyperuricosuria promoting crystallization

Uric acid stones

- Pathogenesis: increase urine acidity plus hyperuricosuria promoting crystallization

- Usually seen in patients w/ Gout, Idiopathic Uric Acid Lithiasis, Dehydration, Metabolic Syndrome (insulin resistance decreasing amniogenesis)

Uric acid stones - Pathogenesis: increase urine acidity plus

hyperuricosuria promoting crystallization - Usually seen in patients w/ Gout, Idiopathic Uric

Acid Lithiasis, Dehydration, Metabolic Syndrome (insulin resistance decreasing amniogenesis)

- uric acid concentration above 100 mg/L, above this level is supersaturation

Uric acid stones - Pathogenesis: increase urine acidity plus

hyperuricosuria promoting crystallization - Usually seen in patients w/ Gout, Idiopathic Uric Acid

Lithiasis, Dehydration, Metabolic Syndrome (insulin resistance decreasing amniogenesis)

- Uric acid concentration above 100 mg/L, above this level is supersaturation

- Treatment:

Uric acid stones Treatment:

1. Raise urine pH (goal 6 to 6.5 pH) K citrate vs NaHCO3

2. Lower Uric acid excretion by diet and Allopurinol

2. Uric acid stones

3. Cystine stones

Cystine Stones - inherited disorder, proximal tubular and jejunal

transport of dibasic amino acids including cysteine

transport of dibasic amino acids including cysteine - Treatment: 1. Hydration approximately 3L/day

transport of dibasic amino acids including cysteine - Treatment: 1. Hydration approximately 3L/day 2. Low salt diet

transport of dibasic amino acids including cysteine

- Treatment:

1. Hydration approximately 3L/day

2. Low salt diet

3. Avoiding high protein diets

2. Uric acid stones

3. Cystine stones

4. Struvite stones

Struvite Stones - result of urinary infection w/ usually Proteus sp.

- Pathogenesis

1. Proteus possess urease degrading urea to NH3 and CO2

- Pathogenesis

2. NH3 hydrolyzes to NH4 raising the urine pH

- Pathogenesis

2. NH3 hydrolyzes to NH4 (which is usually low in urine) raising the urine pH

3. CO2 hydrates to H2CO3 then disocciates to CO3 that precipitates with Ca as CaCO3

Struvite Stones - result of urinary infection w/ usually Proteus sp. - Pathogenesis 1. Proteus possess urease degrading urea to NH3 and CO2 2. NH3 hydrolyzes to NH4 (which is usually low in urine)

raising the urine pH 3. CO2 hydrates to H2CO3 then disocciates to CO3 that

precipitates with Ca as CaCO3 4. NH4 precipitates PO4 and Mg to form MgNH4PO4 or the

struvite

- Pathogenesis

- Treatment

1. Complete removal of stone (percutaneous nephrolithotomy)

- Pathogenesis

- Treatment

1. Complete removal of stone (percutaneous nephrolithotomy sometimes w/ Extracorporeal lithotripsy) w/ subsequent

2. Hemiacidrin (melts struvite stone) – reduces rate of recurrence

3. Antimicrobial for acute infections, culture guided

- Pathogenesis

- Treatment

Urinary Tract ObstructionUrinary Tract Obstruction

Obstruction to the flow of urine w/ stasis and elevation in the urinary tract pressure impairing renal and urinary conduit function

With early relief of obstruction dysfunction disappears

Intrinsic vs Extrinsic mechanical blockade and functional defects (w/o assoc occlusion of urinary drainage)

With early relief of obstruction dysfunction disappears Intrinsic vs Extrinsic mechanical blockade and

functional defects (w/o assoc occlusion of urinary drainage)

Common sites:ureteropelvic, ureterovesical, bladder neck and urethral meatus

With early relief of obstruction dysfunction disappears Intrinsic vs Extrinsic mechanical blockade and

functional defects (w/o assoc occlusion of urinary drainage)

Common sites:ureteropelvic, ureterovesical, bladder neck and urethral meatus

Hydroureter vs Hydronephrosis

1. Etiology

Urinary Tract ObstructionUrinary Tract ObstructionCommon Mechanical Causes: Congenital

Ureter Bladder Outlet Urethra

Ureteropelvic Junction narrowing or obstruction,Ureterovesical junction narrowing or obstruction and reflux, ureterocoele, Retrocaval Ureter

Bladder Neck Obstruction, ureterocoele

Posterior urethral valves, anterior urethral valves, strictures, meatal stenosis, phimosis

Urinary Tract ObstructionUrinary Tract ObstructionCommon Mechanical Causes:Acquired Intrinsic

Calculi, Inflammation, Infection, Trauma, Sloughed papillae, Tumors, Blood clots, uric acid crystals

BPH, Prostate CA, Bladder CA, Calculi, Diabetic Neuropathy, Spinal Cord Diseases, Anticholinergic agents and adrenergic antagonist

Strictures, Tumor, calculi, trauma, phimosis

Urinary Tract ObstructionUrinary Tract ObstructionCommon Mechanical Causes:Acquired Extrinsic

Pregnant Uterus, retroperitoneal fibrosis, aortic aneurysm, uterine leiomyoma, extension of nearby 1’CA, lymphoma, PID, Endometriosis, Surgical ligation

Cervical and colon CA, trauma

Trauma

1. Etiology

2. Pathophysiology

Urinary Tract ObstructionUrinary Tract ObstructionPathophysiology of Bilateral Ureteral Obstruction: Acute

Hemodynamic Effects

Tubule Effects Clinical Features

Renal Bld Flow GFR Medullary Blood Flow Vasodilator Pg

Ureteral and tubule pressures Reabsorption of Na, water and urea

Pain (capsule distention), azotemia, oliguria or anuria

Urinary Tract ObstructionUrinary Tract ObstructionPathophysiology of Bilateral Ureteral Obstruction: Chronic

Hemodynamic Effects

Renal Bld Flow GFR Vasoconstrictor Pg RAS

Medullary Osmolarity Concentrating abilityStructural damages, parenchymal atrophy, Transport of E-lytes

Azotemia, HTN, ADH insensitive polyuria, natriuresis, hyperkalemic, hyperchloremic acidosis

Urinary Tract ObstructionUrinary Tract ObstructionRelease of Obstruction

Hemodynamic Effects

Slow increase in GFR

Tubule pressure Solute load per nephron (urea, NaCl), natriuretic factors

Postobstructive diuresis, potential for volume depletion, E-lyte imbalance due to losses of Na, K, PO4, Mg and water

1. Etiology

2. Pathophysiology

3. Diagnosis

1. Etiology

2. Pathophysiology

3. Diagnosis - difficulty voiding, urine volume change, infection, pain,

distention of bladder, presence of external abnormality like phimosis or stenosis

1. Etiology

2. Pathophysiology

3. Diagnosis - difficulty voiding, urine volume change, infection, pain,

distention of bladder, presence of external abnormality like phimosis or stenosis

- urinalysis: hematuria, pyuria and bacteriuria

1. Etiology

2. Pathophysiology

3. Diagnosis

4. Treatment

Treatment - relief of obstruction (temporary basis:

nephrostomy, ureterostomy, cathetherization)

- remove source of obstruction

- surgical procedure if medical condition permits

- in BPH alpha adrenergic blocker and 5- reductase inhibitors

1. Etiology

2. Pathophysiology

3. Diagnosis

4. Treatment

5. Prognosis

Prognosis - depends on irreversible renal damages

- after 8 weeks of complete obstruction maybe irreversible

- if timely, within 2 weeks return to normal function

- radionuclide scan can predict reversibility

- post obstructive diuresis managed effectively

Vascular Injury to the KidneysVascular Injury to the Kidneys

Vacular Injury To The Kidneys Vacular Injury To The Kidneys

1. Atherosclerotic Renovascular Disease

- estimated approximately 5% of HTN, M>F, 50% bilateral

- Pathogenesis

Atherosclerosis

- Pathogenesis

- Diagnosis: good clinical history, doppler UTZ (reversibility), CT scan (radiocontrast toxicity), MRA (90% sensitivity and 95% specificity), angiogram (gold standard)

CT AngiogramCT Angiogram

Magnetic Resonance AngiogramMagnetic Resonance Angiogram

Renal Artery Angiogram Renal Artery Angiogram

- Pathogenesis

- Diagnosis

- Treatment:

Medical- antihypertensives, statins, anticoagulant

Surgical- indications and prequesites

Indications for RevascularizationIndications for Revascularization

Uncontrolled BP despite maximum therapy

Progressive rise in creatinine

Progressive rise in creatinine> 30% rise in use of ACE/ARB

Progressive rise in creatinine> 30% rise in use of ACE/ARBRecurrent Pulmonary Edema

Prerequisites for RevascularizationPrerequisites for Revascularization

Experienced operator

Experienced operatorPresence of two kidneys

Experienced operatorPresence of two kidneysRI < 0.8 in target kidneys

2. Hypertension Clinical Presentation

Essential HTN Malignant HTN

Hypertensive for long period (BP> 150/90), but has not progressed to malignant HTN

Not usually known hypertensive, sudden accelerated HTN (DBP > 130 mmHg), accompanied by papilledema, CNS manifestations

HypertensionHypertension

Afferent arterioles have thickened walls due to eosinophilic homogenous material deposition (hyaline arteriosclerosis)

1. Afferent arterioles w/ fibrin necrosis and eosinophilic infiltration2. Interlobular artery w/ concentric hyperplastic proliferation of the cellular elements of the vascular wall w/ collagen deposition (onion skin lesion)

Afferent arterioles have thickened walls due to eosinophilic homogenous material deposition (hyaline arteriosclerosis)

1. Afferent arterioles w/ fibrin necrosis and eosinophilic infiltration2. Interlobular artery w/ concentric hyperplastic proliferation of the cellular elements of the vascular wall w/ collagen deposition (onion skin lesion)

Older age group, discovered HTN on routine exam, but some may have recurrent head and nape pains, on PE may reveal changes in the retina (arteriolar narrowing and/or flame shaped hemorrhages), renal involvement manifesting as Screa, moderate proteinuria, small kidneys in late stages

Can most likely develop in a previously HTNsive patient, usually 3rd or 4th decade, presenting symptoms usually neurologic, cardiac decompensation and renal failure after, kidneys may not show evidence of chronicity

2. Hypertension Clinical Presentation

Treatment: Control of Hypertension

Nephrolithiasis, Urinary Tract Obstruction, Vascular Injury to the Kidneys

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