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 Bladder Outlet Urethra

Ureteropelvic Bladder Neck Posterior urethral

Junction narrowing Obstruction, valves, anterior
or obstruction, ureterocoele urethral valves,
Ureterovesical strictures, meatal
junction narrowing or stenosis, phimosis
obstruction and
reflux, ureterocoele,
Retrocaval Ureter
 
 Urinary Tract Obstruction
Common Mechanical Causes:Acquired Intrinsic

Ureter Bladder Outlet Urethra

Calculi, BPH, Prostate CA, Strictures, Tumor,

Inflammation, Bladder CA, calculi, trauma,
Infection, Trauma, Calculi, Diabetic phimosis
Sloughed papillae, Neuropathy, Spinal
Tumors, Blood Cord Diseases,
clots, uric acid Anticholinergic
crystals agents and α
adrenergic
antagonist
 Urinary Tract Obstruction
Common Mechanical Causes:Acquired Extrinsic

Ureter Bladder Outlet Urethra

Pregnant Uterus, Cervical and colon Trauma

retroperitoneal CA, trauma
fibrosis, aortic
aneurysm, uterine
leiomyoma,
extension of nearby
1’CA, lymphoma,
PID, Endometriosis,
Surgical ligation
 Urinary Tract Obstruction
1. Etiology
2. Pathophysiology
 Urinary Tract Obstruction
Pathophysiology of Bilateral Ureteral Obstruction: Acute

Hemodynamic Tubule Effects Clinical Features

Effects

↑ Renal Bld Flow ↑ Ureteral and Pain (capsule

↓ GFR tubule pressures distention),
↓ Medullary Blood ↑ Reabsorption of azotemia, oliguria
Flow Na, water and urea or anuria
↑ Vasodilator Pg
 Urinary Tract Obstruction
Pathophysiology of Bilateral Ureteral Obstruction: Chronic

Hemodynamic Tubule Effects Clinical Features

Effects

↓ Renal Bld Flow ↓ Medullary Azotemia, HTN,

↓ ↓ GFR Osmolarity ADH insensitive
↑ Vasoconstrictor ↓ Concentrating polyuria,
Pg ability natriuresis,
↑ RAS Structural hyperkalemic,
damages, hyperchloremic
parenchymal acidosis
atrophy,
↓ Transport of E-
lytes
 Urinary Tract Obstruction
Release of Obstruction

Hemodynamic Tubule Effects Clinical Features

Effects

Slow increase in ↓ Tubule pressure Postobstructive

GFR ↑ Solute load per diuresis, potential
nephron (urea, for volume
NaCl), natriuretic depletion, E-lyte
factors imbalance due to
losses of Na, K,
PO4, Mg and water
 Urinary Tract Obstruction
1. Etiology
2. Pathophysiology
3. Diagnosis
 Urinary 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 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 Obstruction
 Urinary Tract Obstruction
1. Etiology
2. Pathophysiology
3. Diagnosis
4. Treatment
 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. Etiology
2. Pathophysiology
3. Diagnosis
4. Treatment
5. 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 BP despite maximum
therapy
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
1. Atherosclerotic Renovascular
Disease
2. Hypertension
Clinical Presentation
 Hypertension
Essential HTN Malignant HTN

Hypertensive for long period (BP> Not usually known hypertensive,

150/90), but has not progressed to sudden accelerated HTN (DBP >
malignant HTN 130 mmHg), accompanied by
papilledema, CNS manifestations

 
 Hypertension
Essential HTN Malignant HTN
Hypertensive for long period (BP> 150/90), but has Not usually known hypertensive, sudden
not progressed to malignant HTN accelerated HTN (DBP > 130 mmHg), accompanied
by papilledema, CNS manifestations

Afferent arterioles have 1. Afferent arterioles w/ fibrin

thickened walls due to necrosis and eosinophilic
eosinophilic homogenous infiltration
material deposition (hyaline 2. Interlobular artery w/
arteriosclerosis) 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 Not usually known hypertensive, sudden accelerated HTN (DBP >
to malignant HTN 130 mmHg), accompanied by papilledema, CNS manifestations

Afferent arterioles have thickened walls due to eosinophilic 1. Afferent arterioles w/ fibrin necrosis and eosinophilic infiltration
homogenous material deposition (hyaline arteriosclerosis) 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 Can most likely develop in a previously
routine exam, but some may have HTNsive patient, usually 3rd or 4th decade,
recurrent head and nape pains, on PE presenting symptoms usually neurologic,
may reveal changes in the retina cardiac decompensation and renal failure
(arteriolar narrowing and/or flame shaped after, kidneys may not show evidence of
hemorrhages), renal involvement chronicity
manifesting as ↑ Screa, moderate
proteinuria, small kidneys in late stages
Vacular Injury To The Kidneys
1. Atherosclerotic Renovascular
Disease
2. Hypertension
Clinical Presentation
Treatment: Control of Hypertension