Nephrolithiasis Flashcards
dietary factors that lead to nephrolithiasis
low fluid intake, calcium, K
high oxalate, protein, Na, sugar drinks
hipercalciuria= droga =tiazidicos-diminuir proteina, sodio, acucar e ingesta de calcio adequada
hiperoxaluira-diminuir a ingestao de oxalato, aumentar a ingesta de calcio,evitar vitamina c- piridoxina
hiperuricosuria= evitar purinas= inibidor da xantila oxilase
hipocitraturia= citrato de k, diminuir a ingesta de proteina, aumentar ingesta de frutas e vegetais
Inhibitors of stone formation
magnesium
, citrate
, pyrophosphate→retards the crystal growth of CaP and CaOx crystals by binding to the surface of basic CaP crystals
THprotein
acts as both promoter and inhibitor of stone formation THProtein
THProtein
Tamm-Horsfall protein and uromodulin are two names for the same gene.
Casts only form in the distal tubule & collecting duct, not in the proximal tubule. What is its function?
- Tamm-Horsfall protein acts as a constitutive inhibitor of calcium-based stone formation. Mice deficient for Tamm-Horsfall protein show an increased tendency towards nephrolithiasis.
- Tamm-Horsfall protein acts to prevent urinary tract infection. There is some data that certain strains of E. coli may be bound by Tamm-Horsfall protein; once cleaved this could represent a means of eliminating the organism from the urinary tract.
- Mutations in Tamm-Horsfall protein cause the autosomal dominant disorder medullary cystic kidney disease type 2 (MCDK2) as well as the disorder familial juvenile hyperuricemic nephropathy (FJHN) . This is a pediatric-onset disease characterized by hyperuricemia, gout, and progressive renal failure. Interestingly it appears that the pathophysiologic mechanism here is that mutations in this gene lead to defects in protein folding and intracellular deposition of mutant Tamm-Horsfall protein.
metabolic processes that induce ca stone formation
Increase urine ca >250-300 mg/day;
Urine Uric acid > 800 mg/day
, urine oxalate > 45 mg/d
, hipocitraturia < 320 mg/day;
alterations in urine ph
most common metabolic abnormality in ca stone formation
absorptive hypercalciuria
most common cause of resoprtive hypercalciuria primary hyperparathyroidism
uso de tiazidicos se hipercalciuria >200
clinical conditions with hypocitraturia
overproduction acidosis,
underexcretion acidosis
K deficiency
excess dietary protein
inflammatory bowel disease, jejunoileal bypass, bariatric surgery for morbid obesity
enteric hyperoxaluria
predispose to caphos lithiasis
alkaline urine (pH > 6.7)
most impt in uric acid stones
low urine pH
Uric Acid crystals
Precipitate in acid urine • Pleomorphic,rhombic plates or rosettes. • Seen under polarised light • Hyperuricemia • Diabetes mellitus • Metabolic syndrome • Acute uric acid nephropathy • Chronic uratenephropathy • Familial Juvenile Hyperuricemic Nephropathy (Medullary Cystic Kidney disease
Alkalinization of urine—urine pH is most important risk factor for uric acid stones – Potassium citrate or bicarbonate – Patient follow urine pH (aim for ~6.5 or higher
patients with gouty arthritis and kidney stones, UA > 10 md/d, urine ua > 1000 mg/day
hyperuricosuria
Increases saturation of all stone forming elements
low urine volume
Pathophysio of uric acid stones
Low urine pH, volume
Hyperuricosuria
genetic disease caused by inactivating mutations of the subunits of a dibasic aminoacid transporter in then proximal tubule
cystinuria
family hx of cystinuria (> 400 mg/day vs 30 mg), staghorn calculi, hexagonal crystals on urinalysis
most prevalent component of kidney stones
calcium oxalate
most likely cause of nephrolithiasis in a patient with distal RTA
hypocitraturia
depressions near the papillary tips, yellow crystalline deposits in the ducts of bellini, some randall plaques
Calcium phosphate
1st kidney stone work up
medical hx, stone analysis, urine analysis
Recurrent kidney stone
full metabolic evaluation - serum panel, PTH, VitD if hyperCa, 24ag urine >= 2 samples Na Ca Oxalate Uric acid citrate
calcio, citrato, oxalato, sodio, creatinina,acido urico
Complete Metabolic Evaluation for Nephrolithiasis
Blood
Serum calcium (if elevated, suggests primary hyperparathyroidism or other cause of hypercalcemia)Serum electrolytes (low total CO
2
raises the possibility of distal RTA)
Urine
Urinalysis—urine pH >7 with phosphate crystals in the urine sediment suggests calcium phosphate or struvite stones (struvite stones have a typical coffin-lid appearance); hexagonal cystine crystals arediagnostic of cystinuria; other crystals (calcium, uric acid, indinavir, etc.) may suggest etiology of stones24-hour urine collection(s) for urine stone risk diagnostic profile. This test is now standardized in mostclinical laboratories, with most using a reference laboratory that provides a graphical display of results(seeFig. 20
indicative of minimal fluid intake
urine volume less than 2.5L
pH with increase risk of uric acid precipitation, idiopathic uric acid stone, intestinal disease and diarrhea and intestinal bypass surgery
less than 5.5
Increase risk of caphos precipitation, dRTa, primary hyperparathyroidism, alkali, ca tx
pH > 6.7
pH that indicates urinary tract infection fom urease producing bacteria
> 7-7.5
Normal UCrea
F: 15-20 mk
M: 20-25 mk
reflects dietary Na and K intake
24H urine Na and K
O valor obtido em mEq/24h deve ser dividido por por 17 (Já que 1 g de NaCl corresponde a 17 mEq de sódio, dividimos o resultado por 17 para obter a quantidade em gramas de NaCl consumido no dia).
3- O KDIGO (Kidney Disease Improving Global Outcomes) de Hipertensão e Doença renal crônica, recomenda a ingestão < 2g de Sódio ou 5 gramas de NaCl por dia.
Major cause of hypercalciuria
High Na intake
Normal Urine Na K Ca
Na 100 K 40-60 Ca < 250-300 mg
Low Mg increases risk of
calcium stones
(UMg <30-120 mg)
Higher Uphos > 1100 mg
calcium phosphate formation
hyperuricosuria, Uuric acid > 600-800
CaOx stones Uph > 5.5
Uric acid stones UpH <5.5
marker of dietary acid intake
sulfate
high ammonium/sulfate ratio
GI alkali loss
Normal Urine NH4
30-40 meq