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Urinary lithiasis. The 3rd most common disorder of urinary tract after UTI & prostate disorders. Without medical intervention stone recurrence rate after surgery can be as high as 50% within 5yr
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The 3rd most common disorder of urinary tract after UTI & prostate disorders. Without medical intervention stone recurrence rate after surgery can be as high as 50% within 5yr *Stone occurrence is relatively uncommon before age 20 but peaks in incidence in the fourth to sixth decades of life *men are affected 2-3 times more frequently than women
Etiology If urinary constituents are similar in each kidney and if there is no evidence of obstruction, why do most stones present in a unilateral fashion? Why don’t small stones pass uneventfully down the ureter early in their development? Why do some people form one large stone and others form multiple small calculi? The etiology remain speculative
The physical process of stone formation is a complex cascade of events that occurs as the glomerular filtrate traverses the nephron. It begins with urine that becomes supersaturated with respect to stone-forming salts lead to crystal formation. crystals may flow out with the urine or become retained in the kidney at anchoring sites that promote growth and aggregation, ultimately leading to stone formation
pure aqueous solution of a salt is consideredsaturated when it reaches the point at which further added salt crystals will not dissolve In urine, despite concentration products of stone-forming salt components, such as calcium oxalate, that exceed the solubility product, crystallization does not necessarily occur because of the presence of inhibitors and other molecules
Nucleation and Crystal Growth, Aggregation, and Retention Crystal components are the main component of urinary stone the noncrystalline part or Matrix component only 2-10% of the weight. (mainly protein) *Nuclei are the earliest crystal structure that will not dissolve Magnesium and citrate inhibit crystal aggregation. Nephrocalcin, an acidic glycoprotein made in the kidney, inhibits calcium oxalate nucleation, growth, and aggregation
1- Mass precipitation theory suggests that the distal tubules or collecting ducts, or both, become plugged with crystals, thereby establishing an environment of stasis, & further stone growth. This explanation is unsatisfactory; tubules are conical in shape and enlarge as they enter the papilla, thereby reducing the possibility of ductal obstruction.
2- Randalls hypothesis (fixed particle theory) formed crystals are somehow retained within cells or beneath tubular epithelium. Randall noted whitish-yellow precipitations of crystalline substances occurring on the tips of renal papillae as submucosal plaques. 3- Carr hypothesis calculi form in obstructed lymphatics and then rupture into adjacent fornices of a calyx. Arguing against Carr’s theory are the grossly visible early stone elements in areas remote from fornices.
Urinary Ions A. CALCIUM major ion present in urinary crystals over 95% of the calcium filtered at the glomerulus is reabsorbed at both the proximal and distal tubules and limited amounts in the collecting tube. Less than 2% is excreted in the urine. B. OXALATE 10–15% of oxalate found in the urine originates from the diet; the vast majority is a metabolic by product
C. PHOSPHATE important buffer and complexes with calcium in urine. It is a key component in calcium phosphate and magnesium ammonium phosphate stones. The excretion of urinary phosphate in normal adults is related to the amount of dietary phosphate (especially in meats, dairy products, and vegetables) D. URIC ACID Uric acid is the by-product of purine metabolism E. SODIUM sodium plays an important role in regulating the crystallization of calcium salts in urine
F. CITRATE key factor affecting the development of calcium urinary stones. A deficiency commonly is associated with stone formation in those with chronic diarrhea or renal tubular acidosis type I (distal tubular defect) and in patients undergoing chronic thiazide therapy G. MAGNESIUM lack of dietary magnesium is associated with increased calcium oxalate stone formation and calcium oxalate crystalluria H. SULFATE They can complex with calcium & may help prevent urinary calculi.
stone varieties A-Calcium calculi. Calcification either orthtopic in normal places or heterotopic in abnormal places which (dystrophic normal s. calcium or meastatic elevated s calcium) *80-85% of urinary stones are calcareous. Usually due to elevated urinary calcium, uric acid or oxalate or decreased level of urinary citrate. Approximately 1/3rd of pt. undergo metabolic evaluation have no identifiable metabolic defect.
Nephrocalcinossis. Calcification within renal parenchyma, rarely cause symptoms & not amenable to traditional therapy for urinary stone disease. May associated with nephrolithaiasis. Causes; RTA, hyperparathyrodism, medullary sponge kidney, sarcoidosis, milke alkali syndrome, & multiple myeloma.
Types of calcium stone 1-absorptive hypercalciuric nephrolithiasis Due to increase calcium absorption from small bowel predominantly the jejunum resulting in hypercalciuria (>4mg/kg) or (>150-200mg/24hr). Its of 3types; type1-dietary independent (15%) *Cellulose phosphate- binding ca. in bowel prevent its absorption. *hydrochlorothiazides-reduce renal excretion of ca. Type 2- dietary dependent common cause calcium restricted diet (no specific therapy)
Type3-phosphate renal leak (5%) lead to decrease serum phosphate—increase V D3 synthesis—increase ca absorption &excretion. 2-resorptive hypercalciuria; hyperparathyrodism 50% presented with renal stone. suspected in Pt. with ca. phosphate stone, women with recurrent ca. stones & those with both nephrocalcinosis & nephrolithiasis . Hypercalcemia is most consistent sign. 3-Renal induced hypercalciuria. Intrinsic renal tubular defect in ca. excretion. lead to secondary hyperparathyroidism effectively treated by hydrochlorthiazide.
4-Hyperuricosuric calicium nephrolithiasis: Due to either excessive dietary intake of purines or increase endogenous uric acid production *Monosodium urate absorb & adsorb urinary inhibitors & facilitate heterogeneous nucleation. *pt. have elevated urinary uric acid >600-750 mg/24hr. & consistently ph >5.5. The urinary ph help to differentiate hyperuricosuric calcium from hyperuricosuric uric acid nephrolithiasis. -Effectively treated by low purine diet pot.cit. & allopurinol (xanthine oxidase inhibitor) for both exogenous &endogenous respectively.
5-Hyperoxaluric calcium nephrolithiasis: Increase urinary oxalate >40mg/24hr In pt. with inflammatory bowel disease & chronic diarrheal state —malabsorption increase luminal fat & bile, ca bind fat (saponification) no more ca ready to bind oxalate– increase absorption of oxalate (enteric hyperoxaluria) treated by oral ca. or magnesium. Primary hyperoxaluria. rare hereditary disease (enzyme deficiency) ase ca. oxalate stone & nephrocalcinosis. need combined liver &renal transplant.
6-Hypocitrateuric ca.nephrolithiasis. Increase metabolic demand on the renal cell mitochondria decrease the excretion of citrate (hypocitraturia <320mg/24hr) like metabolic acidosis (in RTA), hypokalemia (thiazide therapy), fasting, hypomagnesemia UTI & androgens. In contrast alkalosis, estrogen ,growth h. & V D increase urinary citrate. It complex with ca. ion decreasing energy for crystallization. Treated by potassium citrate.
B. Non calcium calculi. 1- Struvite. composed of MAP (magnesium, ammonium, & phosphate). Infection stone ase urea splitting organisms (proteus, pseudomonas providencia, klebsiella, staph. & mycoplasma.) Most commonly in women & may recur rapidly. usually staghorn calculus. The high ammonium concentration derived from urea splitting lead to alkaline urinary ph ranges from 6.8-8.3 *normal urinary ph=5-7 in which MAP crystal soluble.
2- Uric acid stone Less than 5% of all urinary stones usually in men. Specially pt. with gout, myeloproliferative disease, rapid weight loss, & those treated with cytotoxic drugs. Most of them have no hyperuricemia. Urinary ph consistently < 5.5, in contrast to pt. with hyperuricosuric calcium nephrolithiasis. as urinary ph increase >5.75 it dissociates to soluble urate ion. Treated by increase fluid intake >2L/d & urinary Ph > 6.0 (alkalinization) allopurinol also help reduce uric acid excretion.
3-cystine Secondary to inborn error of metabolism. Resulting in an abnormal intestinal & renal absorption of amino acid cystine, ornithine, lysine, & arginine. Cystine lithiasis is the only clinical manifestation of this defect. The solubility of cystine is ph dependent with dissociation constant pka of 8.1so treated by increase fluid intake >3L & alkalinization. there is no known inhibitor for cystine stone. penicillamine can reduce urinary cystine level it complexes with amino acid—more soluble.
4-Xanthine. Are secondary to congenital deficiency of xanthine oxidase. This enzyme normally catalyzes the oxidation of hypoxanthine to xanthine & xanthine to uric acid. Treatment: high fluid intake, alkalinization trial of allopurinol xanthine oxidase inhibitor?? 5-Other rare indinavir (protease inhibitor) used in treatment of AIDS . Long term used of antacid—silica stone. Triamterene stone ase antihypertensive contain triamterene such as diazyde.
DIAGNOSTIC EVALUATION OF NEPHROLITHIASIS Any evaluation should be able to identify associated metabolic disorders responsible for recurrent stone disease. These metabolic problems include -distal renal tubular acidosis, -primary hyperparathyroidism, -enteric hyperoxaluria, -cystinuria, and -gouty diathesis. medical therapy is indicated not only to prevent further stone formation but also to correct the underlying physiologic disturbance
Indications for a Metabolic Stone Evaluation Recurrent stone formers Strong family history of stones Intestinal disease (particularly chronic diarrhea) Pathologic skeletal fractures Osteoporosis History of urinary tract infection with calculi Personal history of gout Solitary kidney Anatomic abnormalities Renal insufficiency Stones composed of cystine, uric acid, or struvite
Protocol for Low-Risk Single Stone Formers medical history any underlying conditions that may have contributed to the stone disease patient's dietary habits, including fluid consumption and excessive intake of certain foods as well as all medications taken blood screen calcium, sodium, potassium, chloride, carbon dioxide, blood urea nitrogen, creatinine, PTH, uric acid Urinalysis pH, crystalluria, urine culture Radiography Stone analysis
Extensive Diagnostic Evaluation History and physical examination, diet history, radiologic evaluation, two 24-hour urine specimens on random diet, and dietary instruction for restricted diet Urine for pH, Total Volume, Oxalate, Citrate, Qualitative Cystine Blood for PTH, Calcium, Uric Acid, Creatinine, Sodium
CONSERVATIVE MEDICAL MANAGEMENT Fluid Recommendations increase in fluid intake to achieve a daily urine output of 2 liters Lemonade and orange juice increase urine volume as well as increase urinary citrate excretion Increase intake of soda can confer an increased risk of subsequent stone recurrence
Protein Restriction -the incidence of renal stones is higher in populations in which there is an increased animal protein intake -Protein intake increases urinary calcium, oxalate, and uric acid excretion and increase probability of stone formation even in normal subjects -ingestion of protein is second only to ingestion of vitamin D in enhancing intestinal absorption of calcium
Sodium Restriction -Sodium restriction has been widely recommended as an important element of dietary prevention of recurrent nephrolithiasis -The net effect of a high sodium diet was an increased propensity for the crystallization of calcium salts in urine -In combination with animal protein restriction and moderate calcium ingestion, a reduced sodium diet will decrease stone episodes by approximately 50%
Obesity -increased body mass index, larger waist size, and weight gain correlated with an increased risk of stone episodes. This increased stone risk was still more pronounced for women than for men -urine pH appears to be directly correlated with body size so the increased incidence of uric acid stone formation in obese stone formers may be secondary to the production of more acidic urine than in “normal-sized” patients -weight-reducing diet (low-carbohydrate) delivers a marked acid load to the kidney & predispose to increased stone risk
Dietary Calcium Older recommendations to significantly restrict calcium intake probably led to an increase in available intestinal oxalate. As a result, increase oxalate absorption, thereby raising the supersaturation of calcium oxalate Oxalate Avoidance Since less than 10% to 15% of urinary oxalate is usually derived from dietary sources, it is unclear how helpful it is to promote the strict avoidance of oral oxalate loading -avoid foodstuffs that are rich in oxalate, such as spinach, beets, chocolate, nuts, and tea
