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NephrolithiasisNephrolithiasis
Vimar A. Luz, MD, FPCP, DPSNCenter for Renal Diseases
St. Luke’s Medical Center
NephrolithiasisNephrolithiasis
Most common urological problems
NephrolithiasisNephrolithiasis
Most common urological problems13% in men, 7% in women, increasing
in the industrialized world
NephrolithiasisNephrolithiasis
Most common urological problems13% in men, 7% in women, increasing
in the industrialized worldPathogenesis
NephrolithiasisNephrolithiasis
Pathogenesis
1. Breakdown of balance between solubility and precipitation of salts
NephrolithiasisNephrolithiasis
Pathogenesis
1. Breakdown of balance between solubility and precipitation of salts
balanced during adaptation to diet, climate and activity, and also mechanisms of kidneys in inhibiting
crystallization
NephrolithiasisNephrolithiasis
Pathogenesis
1. Breakdown of balance between solubility and precipitation of salts
2. Supersaturation
NephrolithiasisNephrolithiasis
Pathogenesis 1. Breakdown of balance between solubility
and precipitation of salts 2. Supersaturation Metastably supersaturated Upper Limit of Metastability Excessive Supersaturation
NephrolithiasisNephrolithiasis
Pathogenesis 1. Breakdown of balance between
solubility and precipitation of salts 2. Supersaturation 3. Crystallization
NephrolithiasisNephrolithiasis
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
NephrolithiasisNephrolithiasis
Most common urological problems13% in men, 7% in women, increasing
in the industrialized worldPathogenesisDiagnosis
NephrolithiasisNephrolithiasis
Diagnosis
1. S/Sx: flank, lower abdominal, gross or micro hematuria
2. CT scan
3. Ultrasound not as sensitive as CT
4. Abdominal Xrays
NephrolithiasisNephrolithiasis
Most common urological problems13% in men, 7% in women, increasing
in the industrialized worldPathogenesisDiagnosis
Types of stones
NephrolithiasisNephrolithiasis
Types of Stones
NephrolithiasisNephrolithiasis
Types of Stones 1. Calcium stones
NephrolithiasisNephrolithiasis
Types of Stones 1. Calcium stones
- Ca oxalate and Ca phosphate stones 75 to 85% and admixed in the same stone
NephrolithiasisNephrolithiasis
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
NephrolithiasisNephrolithiasis
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
NephrolithiasisNephrolithiasis Idiopathic Calciuria
- most common abnormality found in nephrolithiasis
- familial, can be poly and monogenic
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
NephrolithiasisNephrolithiasis
Types of Stones 1. Calcium stones
2. Uric acid stones
NephrolithiasisNephrolithiasis
Uric acid stones
- Pathogenesis: increase urine acidity plus hyperuricosuria promoting crystallization
NephrolithiasisNephrolithiasis
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)
NephrolithiasisNephrolithiasis
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
NephrolithiasisNephrolithiasis
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:
NephrolithiasisNephrolithiasis
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
NephrolithiasisNephrolithiasis
Types of Stones 1. Calcium stones
2. Uric acid stones
3. Cystine stones
NephrolithiasisNephrolithiasis
Cystine Stones - inherited disorder, proximal tubular and jejunal
transport of dibasic amino acids including cysteine
NephrolithiasisNephrolithiasis
Cystine Stones - inherited disorder, proximal tubular and jejunal
transport of dibasic amino acids including cysteine - Treatment: 1. Hydration approximately 3L/day
NephrolithiasisNephrolithiasis
Cystine Stones - inherited disorder, proximal tubular and jejunal
transport of dibasic amino acids including cysteine - Treatment: 1. Hydration approximately 3L/day 2. Low salt diet
NephrolithiasisNephrolithiasis
Cystine Stones - inherited disorder, proximal tubular and jejunal
transport of dibasic amino acids including cysteine
- Treatment:
1. Hydration approximately 3L/day
2. Low salt diet
3. Avoiding high protein diets
NephrolithiasisNephrolithiasis
Types of Stones 1. Calcium stones
2. Uric acid stones
3. Cystine stones
4. Struvite stones
NephrolithiasisNephrolithiasis
Struvite Stones - result of urinary infection w/ usually Proteus sp.
NephrolithiasisNephrolithiasis
Struvite Stones - result of urinary infection w/ usually Proteus sp.
- Pathogenesis
1. Proteus possess urease degrading urea to NH3 and CO2
NephrolithiasisNephrolithiasis
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 raising the urine pH
NephrolithiasisNephrolithiasis
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
NephrolithiasisNephrolithiasis
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
NephrolithiasisNephrolithiasis
Struvite Stones - result of urinary infection w/ usually Proteus sp.
- Pathogenesis
- Treatment
1. Complete removal of stone (percutaneous nephrolithotomy)
NephrolithiasisNephrolithiasis
Struvite Stones - result of urinary infection w/ usually Proteus sp.
- 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
NephrolithiasisNephrolithiasis
Struvite Stones - result of urinary infection w/ usually Proteus sp.
- Pathogenesis
- Treatment
Urinary Tract ObstructionUrinary Tract Obstruction
Vimar A. Luz, MD, FPCP, DPSNCenter for Renal Diseases
St. Luke’s Medical Center
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
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
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)
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)
Common sites:ureteropelvic, ureterovesical, bladder neck and urethral meatus
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)
Common sites:ureteropelvic, ureterovesical, bladder neck and urethral meatus
Hydroureter vs Hydronephrosis
Urinary Tract ObstructionUrinary Tract Obstruction
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
Ureter Bladder Outlet Urethra
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
Ureter Bladder Outlet Urethra
Pregnant Uterus, retroperitoneal fibrosis, aortic aneurysm, uterine leiomyoma, extension of nearby 1’CA, lymphoma, PID, Endometriosis, Surgical ligation
Cervical and colon CA, trauma
Trauma
Urinary Tract ObstructionUrinary Tract Obstruction
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
Tubule Effects Clinical Features
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
Tubule Effects Clinical Features
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
Urinary Tract ObstructionUrinary Tract Obstruction
1. Etiology
2. Pathophysiology
3. Diagnosis
Urinary Tract ObstructionUrinary Tract Obstruction
1. Etiology
2. Pathophysiology
3. Diagnosis - difficulty voiding, urine volume change, infection, pain,
distention of bladder, presence of external abnormality like phimosis or stenosis
Urinary Tract ObstructionUrinary Tract Obstruction
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
Urinary Tract ObstructionUrinary Tract Obstruction
Urinary Tract ObstructionUrinary Tract Obstruction
1. Etiology
2. Pathophysiology
3. Diagnosis
4. Treatment
Urinary Tract ObstructionUrinary Tract Obstruction
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
Urinary Tract ObstructionUrinary Tract Obstruction
1. Etiology
2. Pathophysiology
3. Diagnosis
4. Treatment
5. Prognosis
Urinary Tract ObstructionUrinary Tract Obstruction
Prognosis - depends on irreversible renal damages
Urinary Tract ObstructionUrinary Tract Obstruction
Prognosis - depends on irreversible renal damages
- after 8 weeks of complete obstruction maybe irreversible
Urinary Tract ObstructionUrinary Tract Obstruction
Prognosis - depends on irreversible renal damages
- after 8 weeks of complete obstruction maybe irreversible
- if timely, within 2 weeks return to normal function
Urinary Tract ObstructionUrinary Tract Obstruction
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
Urinary Tract ObstructionUrinary Tract Obstruction
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
Vimar A. Luz, MD, FPCP, DPSNCenter for Renal Diseases
St. Luke’s Medical Center
Vacular Injury To The Kidneys Vacular Injury To The Kidneys
1. Atherosclerotic Renovascular Disease
Vacular Injury To The Kidneys Vacular Injury To The Kidneys
1. Atherosclerotic Renovascular Disease
- estimated approximately 5% of HTN, M>F, 50% bilateral
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
Vacular Injury To The Kidneys Vacular Injury To The Kidneys
1. Atherosclerotic Renovascular Disease
- estimated approximately 5% of HTN, M>F, 50% bilateral
- 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
Vacular Injury To The Kidneys Vacular Injury To The Kidneys
1. Atherosclerotic Renovascular Disease
- estimated approximately 5% of HTN, M>F, 50% bilateral
- Pathogenesis
- Diagnosis
- Treatment:
Medical- antihypertensives, statins, anticoagulant
Surgical- indications and prequesites
Indications for RevascularizationIndications for Revascularization
Uncontrolled BP despite maximum therapy
Indications for RevascularizationIndications for Revascularization
Uncontrolled BP despite maximum therapy
Progressive rise in creatinine
Indications for RevascularizationIndications for Revascularization
Uncontrolled BP despite maximum therapy
Progressive rise in creatinine> 30% rise in use of ACE/ARB
Indications for RevascularizationIndications for Revascularization
Uncontrolled BP despite maximum therapy
Progressive rise in creatinine> 30% rise in use of ACE/ARBRecurrent Pulmonary Edema
Prerequisites for RevascularizationPrerequisites for Revascularization
Experienced operator
Prerequisites for RevascularizationPrerequisites for Revascularization
Experienced operatorPresence of two kidneys
Prerequisites for RevascularizationPrerequisites for Revascularization
Experienced operatorPresence of two kidneysRI < 0.8 in target kidneys
Vacular Injury To The Kidneys Vacular Injury To The Kidneys
1. Atherosclerotic Renovascular Disease
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
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
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)
HypertensionHypertension
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
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
HypertensionHypertension
Vacular Injury To The Kidneys Vacular Injury To The Kidneys
1. Atherosclerotic Renovascular Disease
2. Hypertension Clinical Presentation
Treatment: Control of Hypertension