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Urinary tract obstruction & Stones Loin pain & hematuria Principal sites of pathology leading to loin pain • • • • • • • Spinal nerve roots Vertebral column Paraspinal & lumbar muscles Kidneys Renal pelvis / ureters Abdominal aorta Pancreas • Renal pain arises because of rapid stretching or inflammation of renal capsule • Pain from the renal pelvis / ureter is caused by distention & excessive peristaltic contractions • Any back / retroperitoneal structure may give rise to back pain Macroscopic hematuria • May arise from lesions anywhere within the urinary system, kidney, renal pelvis, ureter, bladder, urethra • As few as 5 x 10 6 RBC/ml ; 1ul blood/ml urine can be detected visually as red-coloured urine • Macroscopic hematuria needs to be distinguished from – Red discolouration of urine caused by certain dyes & some drugs – Presence of Haem pigment : intravascular hemolysis (Hb), rhabdomyolysis (myoglobin) – Bleeding from outside the urinary tract; perineum, vagina • Bleeding from the bladder or above cause uniform discoloration of urine • Bleeding from the urethra may cause bleeding separate from the urine or mixed with urine • Hematuria from the renal parenchyma – glomeruli or interstitium – tends to be accompanied by proteinuria, casts, & dismorphic RBC (abnormal morphology) • Bleeding from renal tumors or from lesions in the renal pelvis or below may be isolated or associated with pyuria – particularly with infections. • Macroscopic hematuria from tumors are usually painless, whereas that from calculi / infection is usually associated with pain Pyelonephritis/infections • The formation of stone is usually the result of many metabolic and physiologic disorders contributing to stone formation • Stones in the urinary tract are composed of crystals and matrix skeleton. • Physical factors of stone formation – Supersaturation of the urine with respect to a particular solute, e.g. uric acid, due to increase in excretion or decrease in urine volume. At some point spontaneous nucleation and crystal growth occur – homogenous nucleation. – Urine pH, determines the solubility of ccompounds in the urine. Uric acid & cystine are poorly soluble in acidic media, whereas calcium salts are poorly soluble at an alkaline pH. – Crystalization inhibitors; normal urine contain factors that inhibit formation & growth of crystals – Mg, citrate, pyrophosphate, TPH, glucosamine, nephrocalcin. – Heterogenous nucleation appears to be a major mechanism in stone formation. A small crystal, e.g. uric acid, serves as a nidus on which another compound, e.g. ca-oxalate, precipitates – Infection with urea splitting / urease producing microorganisms Disorders causing stone disease • Gastrointestinal disorders; – Fat malabsorption, IBD, small bowel resection & bypass can cause decreased urinery volumes, hyperoxaluria, hyperuric-aciduria, hypocitrateuria, acidic urine. • Hyperparathyroidism / hypercalcemia – Causes of hypercalcemia (& hypercalciuria) are # • Cancer, immobilization, endocrinopathies, dietary, granulomatous disease, renal, drugs • Vit D increases Ca absorption from intestine – Idiopathic Hypercalciuria. • 24h urine[Ca] > 300mg/24h (men), >250mg/24h (women) • Gout & hyperuricosuria. – May promote Ca-oxalate stones • Epitaxy, ca-oxalate deposits on uric acid / Na-urate crystals as nidus • Urate in urine binds glycosamineglycans, an inhibitor of stone formation • Uric acid promotes the degree of aggregation of precipitated crystals – Uric acid lithiasis; elevated urinary uric acid (24h urinary uric acid), acid urine; • Gout, myeloproliferative disorders • Treatment: alkalinization of urine to pH 6-7 , fluids, allopurinol • Infection with urease producing bacteria urea splitting struvite stones – Proteus in majority; Klebsiella, Pseudomonas, Providencia, Staphylococcus, Ureaplasma urealyticum, rarely E. coli. – More common in patients with ileal conduits, hyperchloremic metabolic acidosis, ureteral dilatation, increased volume of residual urine, decreased renal function • • Obstruction & anatomic abnormalities Drugs. – Acetazolamide causes hyperchloremic metabolic acidosis, transiently elevates urine pH, and reduces citrate excretion – Allopurinol increases xanthine excretion and may produce xanthine stones – Several drugs have limited urine solubility, • May promote stone formation or are absorbed into the crystal matrix of other stone • Triamterene, ceftriaxone, sulfonamides, bactrim, sulindac, phenazopyridine • Other : laxatives, vit D, calcium, • Renal tubular disorders. – Cystinuria, • Inherited disorder of amino acid transport, • associated with increased urinary excretion of cystine, ornithine, lysine, & arginine (COLA) • Limited soloubility of cystine promotes recurrent stones, which are radioopaque, homogeneous, may assume staghorn form • Therapy: high fluid intake, alkalinization of urine to pH 7.5 or more; reduce cystine excretion by low Na diet, D-penicillamine, trioponine, captopril (drugs with sulfhydryl) – Distal RTA • Alkaline urine, hypocitrateuria,hypercalciuria – Hyperphosphaturia, causing hypophosphatemia & elevated 1,25-(OH)2D3, hypercalcemia – Idiopathic hypercalciuria; reduced tubular reabsorption of Ca • Enzymatic defects – Xanthinuria. Deficiency xanthine oxidase • Radiolucent xanthine stones – 2,8-dihydroxyadenine. • Deficiency adeninephosphoribosyl transferase (APRT) • Radiolucent stones, requires infrared / crystallographic analysis • Treatment with allopurinol – Primary hyperoxaluria, • Idiopathic Urolithiasis – Majority of patients – Risk factor profile • Abnormally high excretion of Ca (>4mg/kg/d), uric acid, oxalate, Na • Decrease in several inhibitory solutes • Decreased urine volume! • Ability of urine to inhibit agglomeration improves after treatment with alkali, which increase urinary citrate – Excretion of citrate is decreased by systemic acidosis, depletion of kalium & magnesium, starvation acetazolamide, – Most patients with low urinary citate have RTA, chronic diarrhea, hypokalemia, malabsorption, or high intake of animal protein First stone episode Dietary advice: meat, dairy, salt Fluids; f/u 6-12 months No growth Metabolically active Monitor 1-2 years Urinary risk assessment Dietary/fluid Factors persist hypercalciuria hyperuricosuria Evaluate diet Meat, Ca, Na hypocitric aciduria Evaluate for acidosis, RTA GI Dietary, meat Treatment options Repeat Dietary advice specific dietary Rx & / Reduce meat excess Thiazides allopurinol hyperoxaluria Evaluate for dietary excess malabsorption GI disorders measure oxalate/ glycoliate dietary fat / oxalate restriction K-Citrate B6, PO4 Asymptomatic No Rx Symptomatic Calcium stones Mg/NH4/PO4 stones Symptomatic obstructive Percutaneous extraction + ESWL Cystine (cannot dissolve, or obstructive Small <2cm New stones ESWL <2cm >3cm ureteric stones ESWL Perc upper1/3 lower1/3 ESWL ESWL Extraction laser Rx Acute colic: analgetics, fluids >2cm old stones Perc Uric acid (cannot dissolve/ obstructive) ESWL Often requires Urography Usg 7-dehydrocholesterol Skin Diet UV Cholecalciferol liver 25-hydroxycholecalciferol kidney PTH Hypophosphatemia Calcitriol Small intestine Bone 24,25 D Kidney +PTH Increase CaHPO4 absorption Increase Ca & Po4 release Decrease Ca & PO4 excretion Metabolic activation of vit.D The result is an increase in Ca & PO4 concentration Plasma Ca PTH Bone Kidney Vit.D Reabsorption Phosphate Excretion Release of Calcium & phosphate Ca reabsorption Calcitriol formation Intestinal CaHPO4 absorption Effect of PTH on Ca & phosphate metabolism. Net effect is increase in plasma Ca, with no change or decrease in plasma phosphate concentration Plasma Ca [2+] PTH Cacitriol Increased Ca From bone increased Ca from intestine Plasma Ca increase increased phosphate from bone & intestine increased phosphate excretion in urine Plasma Phosphate unchanged Plasma phosphate Calcitriol Ca from intestine PTH Decreased Ca from bone Plasma [Ca] Slight increased decrease phosphate excretion in urine increase phosphate from intestine Plasma [PO4] increased Increased = systemic disease Serum [calcium] normal Normal Hyperuricosuria Hyperoxaluria No abnormality Urinary calcium = idiopathic hypercalciuria RTA Laboratory investigation • • • • • • • Serum electrolytes, BUN, Cr, Ca, PO4, Uric acid Urinalysis; microscopic exam of fresh specimen Urine culture Nitroprusside test for cystine Urine pH, first AM urine, under oil Stone analysis 24h urine for Cr, Ca, PO4, uric acid, Cystine, oxalate • Radiologic studies, USG, BNO, IVP • Special test as indicated; PTH, Thyroid, Cortisol, etc
