Nephrolithiasis, Urinary Tract Obstruction, Vascular Injury To The Kidneys

Nephrolithiasis

Vimar A. Luz, MD, FPCP, DPSN Center for Renal Diseases St. Luke’s Medical Center

Nephrolithiasis  Most

common urological problems

Nephrolithiasis  Most

common urological problems  13% in men, 7% in women, increasing in the industrialized world

Nephrolithiasis  Most

common urological problems  13% in men, 7% in women, increasing in the industrialized world  Pathogenesis

Nephrolithiasis  Pathogenesis

1. Breakdown of balance between solubility and precipitation of salts

Nephrolithiasis  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

Nephrolithiasis  Pathogenesis

1. Breakdown of balance between solubility and precipitation of salts 2. Supersaturation

Nephrolithiasis  Pathogenesis

1. Breakdown of balance between solubility and precipitation of salts 2. Supersaturation Metastably supersaturated Upper Limit of Metastability Excessive Supersaturation

Nephrolithiasis Pathogenesis

1. Breakdown of balance between solubility and precipitation of salts 2. Supersaturation 3. Crystallization

Nephrolithiasis  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

Nephrolithiasis  Most

common urological problems  13% in men, 7% in women, increasing in the industrialized world  Pathogenesis  Diagnosis

Nephrolithiasis  Diagnosis

1. S/Sx: flank, lower abdominal, gross or micro hematuria 2. CT scan 3. Ultrasound not as sensitive as CT 4. Abdominal Xrays

Nephrolithiasis  Most

common urological problems  13% in men, 7% in women, increasing in the industrialized world  Pathogenesis  Diagnosis Types of stones

Nephrolithiasis  Types

of Stones

Nephrolithiasis  Types

of Stones

1. Calcium stones

Nephrolithiasis  Types

of Stones

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

Nephrolithiasis  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

Nephrolithiasis  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

Nephrolithiasis  Idiopathic

Calciuria

- most common abnormality found in nephrolithiasis

Nephrolithiasis  Idiopathic

Calciuria

- most common abnormality found in nephrolithiasis - familial, can be poly and monogenic

Nephrolithiasis  Idiopathic

Calciuria

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

Nephrolithiasis  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

Nephrolithiasis 

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

Nephrolithiasis 

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

Nephrolithiasis 

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:

Nephrolithiasis  Treatment:

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

Nephrolithiasis  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

Nephrolithiasis 

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)

Nephrolithiasis 

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)

Nephrolithiasis 

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

Nephrolithiasis 

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

Nephrolithiasis  Types

of Stones

1. Calcium stones 2. Uric acid stones

Nephrolithiasis  Uric

acid stones

- Pathogenesis: increase urine acidity plus hyperuricosuria promoting crystallization

Nephrolithiasis  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)

Nephrolithiasis  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

Nephrolithiasis  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:

Nephrolithiasis  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

Nephrolithiasis  Types

of Stones

1. Calcium stones 2. Uric acid stones 3. Cystine stones

Nephrolithiasis  Cystine

Stones

- inherited disorder, proximal tubular and jejunal transport of dibasic amino acids including cysteine

Nephrolithiasis  Cystine

Stones

- inherited disorder, proximal tubular and jejunal transport of dibasic amino acids including cysteine - Treatment: 1. Hydration approximately 3L/day

Nephrolithiasis  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

Nephrolithiasis  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

Nephrolithiasis  Types

of Stones

1. Calcium stones 2. Uric acid stones 3. Cystine stones 4. Struvite stones

Nephrolithiasis  Struvite

Stones

- result of urinary infection w/ usually Proteus sp.

Nephrolithiasis  Struvite

Stones

- result of urinary infection w/ usually Proteus sp. - Pathogenesis 1. Proteus possess urease degrading urea to NH3 and CO2

Nephrolithiasis  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

Nephrolithiasis  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

Nephrolithiasis  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

Nephrolithiasis  Struvite

Stones

- result of urinary infection w/ usually Proteus sp. - Pathogenesis - Treatment 1. Complete removal of stone (percutaneous nephrolithotomy)

Nephrolithiasis  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

Nephrolithiasis  Struvite

Stones

- result of urinary infection w/ usually Proteus sp. - Pathogenesis - Treatment

Urinary Tract Obstruction

Vimar A. Luz, MD, FPCP, DPSN Center for Renal Diseases St. Luke’s Medical Center

Urinary 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 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 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 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 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 Obstruction 1. Etiology

Urinary Tract Obstruction Common Mechanical Causes: Congenital

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

Bladder Outlet Bladder Neck Obstruction, ureterocoele

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

Urinary Tract Obstruction Common Mechanical Causes:Acquired Intrinsic

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

Bladder Outlet

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

Urethra Strictures, Tumor, calculi, trauma, phimosis

Urinary Tract Obstruction Common Mechanical Causes:Acquired Extrinsic

Ureter

Bladder Outlet

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

Cervical and colon CA, trauma

Urethra Trauma

Urinary Tract Obstruction Etiology 2. Pathophysiology 1.

Urinary Tract Obstruction Pathophysiology of Bilateral Ureteral Obstruction: Acute

Hemodynamic Effects ↑ Renal Bld Flow ↓ GFR ↓ Medullary Blood Flow ↑ Vasodilator Pg

Tubule Effects ↑ Ureteral and tubule pressures ↑ Reabsorption of Na, water and urea

Clinical Features Pain (capsule distention), azotemia, oliguria or anuria

Urinary Tract Obstruction Pathophysiology of Bilateral Ureteral Obstruction: Chronic

Hemodynamic Effects ↓ Renal Bld Flow ↓ ↓ GFR ↑ Vasoconstrictor Pg ↑ RAS

Tubule Effects ↓ Medullary Osmolarity ↓ Concentrating ability Structural damages, parenchymal atrophy, ↓ Transport of Elytes

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

Urinary Tract Obstruction Release of Obstruction

Hemodynamic Effects Slow increase in GFR

Tubule Effects

Clinical Features

↓ 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 Obstruction Etiology 2. Pathophysiology 3. Diagnosis 1.

Urinary Tract Obstruction Etiology 2. Pathophysiology 3. Diagnosis - difficulty voiding, urine volume change, infection, pain, 1.

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

Urinary Tract Obstruction Etiology 2. Pathophysiology 3. Diagnosis 1.

- 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 Obstruction

Urinary Tract Obstruction Etiology 2. Pathophysiology 3. Diagnosis 4. Treatment 1.

Urinary 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-α reductase inhibitors

Urinary Tract Obstruction 1. 2. 3. 4. 5.

Etiology Pathophysiology Diagnosis Treatment Prognosis

Urinary Tract Obstruction 

Prognosis - depends on irreversible renal damages

Urinary Tract Obstruction 

Prognosis - depends on irreversible renal damages - after 8 weeks of complete obstruction maybe irreversible

Urinary 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 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 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 Kidneys

Vimar A. Luz, MD, FPCP, DPSN Center for Renal Diseases St. Luke’s Medical Center

Vacular Injury To The Kidneys 1.

Atherosclerotic Renovascular Disease

Vacular Injury To The Kidneys 1.

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

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 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 Angiogram

Magnetic Resonance Angiogram

Renal Artery Angiogram

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 Revascularization  Uncontrolled

therapy

BP despite maximum

Indications for Revascularization  Uncontrolled

BP despite maximum

therapy  Progressive rise in creatinine

Indications for Revascularization  Uncontrolled

BP despite maximum

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

Indications for Revascularization  Uncontrolled

BP despite maximum

therapy  Progressive rise in creatinine  > 30% rise in use of ACE/ARB  Recurrent Pulmonary Edema

Prerequisites for Revascularization  Experienced

operator

Prerequisites for Revascularization  Experienced

operator  Presence of two kidneys

Prerequisites for Revascularization  Experienced

operator  Presence of two kidneys  RI < 0.8 in target kidneys

Vacular Injury To The Kidneys Atherosclerotic Renovascular Disease 2. Hypertension 1.

Clinical Presentation

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

 

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

Hypertension 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 infiltration 2. Interlobular artery w/ concentric hyperplastic proliferation of the cellular elements of the vascular wall w/ collagen deposition (onion skin lesion)

Hypertension 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 infiltration 2. 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

Vacular Injury To The Kidneys Atherosclerotic Renovascular Disease 2. Hypertension 1.

Clinical Presentation Treatment: Control of Hypertension