RENAL STONE DISEASE
Dr. Samir Ali 19th, and 26th of March, 2015Epidemiology
Intrinsic factors age Metabolic and idiopathic, 3rd and 4th decade of life Infection 5th decade Sex Metabolic and idiopathic M>F 3:1 Infection F>M Genetic/familial Stones are more in Asians and Caucasians, and rare in native Americans and Blacks. Having a first degree relative with stone disease doubles the risk for getting it.Extrinsic factors geographical location climate season Water intake diet: high animal protein and refined carbohydrates increase the risk, while fiber rich diet reduces it. Occupation Diseases and drugs: like bowel inflammatory conditions, and antacids.
Stone classification
according to Radiological appearance Radioopaque like calcium phosphate, and calcium oxalate Relatively radioleucent like cystine and struvite Completely radioleucent like uric acid, xanthine, and triamterene Composition Calcareous like calcium oxalate and phosphate Non calcareous like uric acid and cystine Size and shape Single , multiple Amorphous, staghornMechanism of formation: Stone formation requires SUPER-SATURATION Inhibitory crystals: Citrate, mg, THP
Causes
Idiopathic: most common cause Abnormalities of urine: Congenital: primary hyperoxalurea, cystinurea Acquired: dehydration, dietary hypercalciuria Abnormalities of the urinary tract: Cong: PUJ obstruction, ureteroceles, diverticuli Acquired: postoperative or traumatic fibrosisStone Components
Crystal component: >90% Crystal formation occurs in 3 steps: nucleation, growth, and aggregation Nucleation can be either homogenous or hetergenous B. Matrix component:< 10% Protiens, hexose, and hexosamines Matrix role??? Matrix stone:
Urinary Ions
Ca+2: it is the major ion present in urinary stones.50% of plasma ca+2 is ionized and filterable, it’s reabsorbed by PT&DT, 2% excreted.Normal urinary Ca+2 in adults is ≤4mg/kg/day.Diuretics decrease u. ca+2Increased monosodium urate increase ca+2 –oxalate crystallization.Acidic urine increase the crystallization also.Oxalate:
85% is a metabolic by-product, while only 15% is dietary IN BOWEL: either absorbed then exclusively excreted by PT, or metabolized by bacteria, or complex and excreted in feces. Normal level is less than 45 mg/day.Phosphate: is an important buffer that complexes with ca+2 in urine Part of MAP stone Urinary excretion depends on dietary intake (meat), then filtered by the glomerulus and re absorbed by PT under influence of PTH Na+: although it is not a major constituent of urinary stone, it plays a very important role in the regulation of ca+2 salts crystallization, a major increase in u. Na+ excretion will dramatically increase u. Ca+2
Uric acid: is a byproduct of purine metabolism, it’s Pka is 5.75, so its solubility increases in alkaline urineCitrate: is the major stone inhibitor in urine, its level in urine decreases in:Metabolic acidosisRTA type IChronic diarrhoeaThiazide therapyHypokalemiaEsterogen lack in females
Other inhibitors: Mg Sulfate Urinary proteins (Tamm-Horsfall pr.) Pyrophosphate Glycoseamineglycans uropontine
Stone Varieties
Calcium stones (85%)HypercalciuricHyperoxaluricHyperuricoseurichypocitraturicNon calcium stones (15%)Struvite “infection, MAP”Uric acidCystineXanthineOthers: indinavirHypercalciuric
Absorptive: increased calcium absorption from bowel Resorptive: hyperPTH leading to calcium mobilization from its bone reservoires Renal leak of calcium: intrinsic defect in renal tubules.
Hyperoxaluric
Primary hyperoxaluria: a rare AR disease, there is intrinsic hepatic oxalate production, it is aggressive and ends in RF, the definitive therapy by combined renal and liver transplantation. Enteric hyperoxaluria: oxalate is poorly absorbed by intestine, but once absorbed it is exclusively excreted in urine, causes of increased absorption include: IBD, small bowel bypass, mal-absorption syndromes. Oxalate rich foodHyperuricoseuria
High uric acid levels lead to formation of uric acid crystals on the surface of which calcium oxalate crystals form (heterogeneous nucleation) Due to either excessive oral purine intake, or excessive endogenous productionHypocitraturia
Citrate is the major stone inhibitor in urine Causes of hypocitraturia are mentioned before Metabolic acidosis RTA type I Chronic diarrhoea Thiazide therapy hypokalemia Normal level: > 320 mg/24 hrs Treatment: by potassium citrate suppl. 6-8 glasses of lemonade per day increase U. citrate by 150 mg/dayStruvite Stones
Also called triple phosphate, or infection stones Composed of MAP Urease producing bacteria hydrolyses urea into co2 and ammonium, with high PH levels. These include: proteus, pseudomonads, klebsiella and staph. But not E.coli. MAP crystals ppt. only in high PH>7.2 Faintly radioopaque Treatment should include complete removal and control of infection.Uric acid stones
5-10 % of all u. stones Pure uric acid stones are radiolucent Xanthine oxidase converts xanthine into uric acid, this is inhibited by allopurinol. Urinary pH < 5.5 May be formed in patients with: Gout. Myeloproliferative disorders specially on cytotoxics. Chronic dehydration Corner stones of treat included: Good hydration Urine alkalization AllopurinolCystine stones
1-2% of all stone types Have faintly opaque ground glass appearance AR inborn error of metabolism There is decreased renal tubular re-absorption of dibasic amino acids COLA Its PKa is 8.1, so the more alkaline the urine the more cystine is soluble Medical therapy may dissolve or prevent stone recurrence by: Adequate hydration Urine alkalization Cystine binding drugs as penicillamine, captopril, thiola, or bucacillin
Sign and Symptoms
May found incidentally during investigations for other pathologies. Or symptomatic pain Hematuria: microscopic in up to 90% Infection: affects pain perception, endotoxins and exotoxins affect ureteric peristalsis, it may range from simple to frank pyonephrosis (emergency) GI symptoms like nausea and vomitingSite and radiation of pain
Signs: Pain causes sweating, hypotension, tachypnoea and tachycardia Obs,infection,and pyonephrosis cause high temp,rigor and sepsis Renal angle tenderness Bladder may be tender or with urine retention Carry out full abd. exam and exclude other diff.diagnosisDiagnostic tests:
Urinanalysis Renal function test Imaging studies: Abd. US Plain X-ray (KUB) Radiodensity in order: ca-phosphate>ca-oxalate>struvite>>cystine EXU look for function, anatomy, and leucent stones CT scanTreatment of renal stones
Keep in mind: the aims of treatment are firstly to protect/save the kidney, and secondly to make the patient stone free.Decision depends on:Stone size, site, and typeRenal function and anatomyPatient clinical conditionFacility availablePatient’s and doctor’s preferenceKeep in mind, the younger the patient, the larger the stone, the more symptoms, the more incline toward interventionIndications for hospitalization
Modalities
Conservative observation (WW): Small calculi without obstruction need no urgent intervention, and have great chance of spontaneous passage, specially if <7 mm. Analgesia is the corner stone of treatment, the best is indomethasin supp. (Keotrolac??). Anti-emetics AB if associated infection Diuretics and antispasmodics have no role Keep the patient well hydrated but not overhydrated Encourage normal movementIndication for early intervention
High-grade urinary obstruction Persistent infection despite antibiotics Uncontrollable pain Impairment of renal functionESWL
Has revolutionized the stone management Shock waves: unharmonic, with steep rise in pressure amplitude that results in compressive forces. It includes: Energy source: electrohydrolic, electomagnetic, piezoelectric, to create the shock waves Coupling mechanism: transfer the energy into the human body Localization technique: help localize the stone and focus the SW on it, either by US, or flouroscopyPatient preparation:
exclude distal obstruction urinanaysis to exclude infection bleeding profile In some cases ureteric stent (single kidney or large stone burden > 2cm) Contraindication: Pregnancy Uncontrolled bleeding tendency Large abd. aortic aneurysm Distal obstruction Uncontrolled hypertension?????Complications:
Common Hematuria Renal pain infection Occasional Stone does not break requiring alternative treatment Response is partial requiring repeat sessions Rare Hematoma formation Stone gravels stuck in the ureter (stienstrass) Long term effect on renal function and blood pressure is still controversial.Post ESWL care:
Abd. examinationDon’t let the pt. leave before passes urineAnalgesia Adequate oral hydrationInstruct the pt to monitor his urine for stone gravels
Retrograde intrarenal surgery (RIRS)
The development of small caliber flexible ureteroscopes with active deflection and instrument channels in combination with small diameter laser fibers and stone baskets and graspers has opened the way for intracorporeal endoscopic treatment of renal stones Used when ESWL failed or contraindicated, specially lower pole or calyceal stones and obese patients.Percutaneous Nephrolithotomy
Greatly replaced open surgical procedures Done under flouroscopic or ultrasonic guidance creation of a nephrostomy tract toward the targeted calyx, the tract then dilated and used to pass a nephroscope into the collecting system, through which litholapaxy or lithotripsy is done. Mainly used for staghorn calculi, and those who failed ESWL treatment. Advantages: No surgical wound and scar Short hospitalization Less blood transfusionSurgery:
Laparoscopy Transperitoneal retroperitoneal Open surgery Pyelolithotomy Nephrolithotomy Extended pyelo-nephrolithotomy Partial nephrectomy NephrectomyUreteric Stones:
can impact anywhere in the ureter, but mostly in the three normal narrowings: what are these?? Modalities: Conservative, (medical expulsive therapy) provided that the renal function and anatomy are normal. acute management of ureteric colic is as mentioned with renal stones Emergency temporizing measures as JJ stents and PCN. ESWL can be used for all ureteric stones sp. upper, limitation when over bone Ureteroscopy specially after the invention of flexible ones. Open surgery (ureterolithotomy)Vesical Stones
Childrean: Dietary cause: low pr. High CHO diet, formation of ammonium urate stones Urine is sterile Males>females Adults: Obstruction: ca-ox stone e.g: BPH, urethral stricture, neuropathic bladder Urine is infected F.B as stitches Or descended stonePresentation:
Asymptomatic Hesitancy, frequency, dysuria Hematuria Pain referred to tip of penis Urine retention Diagnosis: US, KUB,EXU, CYSTOSCOPY