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Major Nonglomerular Disorders of the Kidney (NEPHROLITHIASIS (Approach…

- - - - incr intake of foods rich in alkali (e.g., fruits and vegetables) and reducing the intake of foods that produce acid (e.g., animal flesh)
      - If necessary, supplementation w/ bicarbonate or citrate salts (preferably potassium citrate);
      - If not successful-->a xanthine oxidase inhibitor, such as allopurinol or febuxostat
  - - - white men: 3.5 cases/1000 at 40 (peak) and declines to ~2 cases/1000 by 70.
      - white women: 2.5 cases/1000 in their 30s; decr to ~1.5/1000 at 50 and beyond
  - - - Ca
      - oxalate
      - Citrate: a natural inhibitor of Ca-containing stones
      - Uric acid
      - pH
        
        Uric acid form only when urine pH is consistently ≤5.5
        
        Ca phosphate more likely to form when urine pH is ≥6.5
        
        Ca oxalate not influenced by urine pH
        
        Cystine more soluble at higher urine pH.
      - Volume
    - - decr risk
        
        Ca: --> reduction in intestinal absorption of dietary oxalate; Low Ca intake is contraindicated; supplemental ca may incr risk
        
        K: decr Ca excretion, and many K-rich foods incr urinary citrate excretion due to alkali content
        
        phytate + Mg
        
        vit B6 supplements: may be beneficial in pxs w/ type 1 primary hyperoxaluria
        
        Fluids and beverages
      - incr risk
        
        animal pr :--> incr excretion of Ca and uric acid + decr urinary excretion of citrate--> all incr risk of stone formation.
        
        oxalate: much of oxalate in food may not be readily absorbed. However, absorption may be higher in stone formers. urinary oxalate is a strong RF for Ca oxalate stone formation
        
        Na + sucrose + fructose : incr Ca excretion independent of Ca intake
        
        Vit C supplements: possibly bc of raised levels of oxalate in urine.
  - - - parenteral NSAIDs (ex ketorolac) just as effective as opioids in relieving symptoms and fewer side effects.
        Excessive fluid administration not shown to be beneficial;
        alpha-blocker may incr rate of spontaneous stone passage (dilates ureter)
      - Urologic intervention postponed unless evidence of UTI, a low probability of spontaneous stone passage (e.g., a stone measuring ≥6 mm or an anatomic abnormality), or intractable pain.
      - Extracorporeal shockwave lithotripsy, least invasive option, to fragment the stone.
        endourologic approach: remove stone by basket extraction or laser fragmentation.
        For large upper-tract stones, percutaneous nephrostolithotomy
    - - Serum typically normal, but WBC count may be elevated.
      - urine sediment: u. RBC + WBC + occasionally crystals; absence of hematuria does not exclude a stone, particularly when urine flow is completely obstructed by a stone.
      - diagnosis often made on basis of Hx, P/E, and urinalysis--> may not be necessary to wait for radiographic confirmation before treating symptoms; diagnosis confirmed by an appropriate imaging study—preferably helical CT (highly sensitive, allows visualization of uric acid stones (traditionally considered “radiolucent”), and is able to avoid radiocontrast); plain abdominal radiograph (kidney/ureter/bladder, or KUB) can miss a stone in ureter or kidney, even if radiopaque, and does not provide info on obstruction. Abdominal ultrasound offers advantage of avoiding radiation and provides info on hydronephrosis, but not as sensitive as CT and images only kidney and possibly proximal segment of ureter; thus most ureteral stones not detectable by ultrasound.
    - - lodged at R ureteral pelvic junction--> acute cholecystitis
      - blocks ureter as it crosses over R pelvic brim--> acute appendicitis
      - blockage at L pelvic brim--> acute diverticulitis
    - - serum levels: electrolytes (hypokalemia or RTA), creatinine, Ca, and uric acid; PTH if indicated by high Ca;
      - examination of urine sediment: in asymptomatic residual renal stones, RBC + WBC frequently present, crystals help stone type
      - 24-h urine collections: cornerstone on which therapeutic recommendations based.
        factors measured: total volume, Ca, oxalate, citrate, uric acid, Na, K, phosphorus, pH, and creatinine
      - Stone composition analysis
- - - - Clinical Features
        rifampin, proton pump inhibitors and, rarely, sulfonamide, antiretrovirals.
        
        classic presentation: fever, rash, peripheral eosinophilia, and oliguric renal failure occurring after 7–10 days of treatment w/ methicillin or another β-lactam antibiotic: is the exception rather than the rule.
        
        More often: found incidentally to have a rising serum creatinine or present w/ symptoms attributable to ARF.
        Atypical reactions can occur, most notably NSAID-induced AIN, in which fever, rash, and eosinophilia are rare, but acute renal failure w/ heavy proteinuria common.
      - Diagnosis: [Finding otherwise unexplained RF and exposure to a potentially offending agent usually points to diagnosis] Peripheral blood eosinophilia adds supporting evidence but present in only a minority of patients. biopsy not required
  - - - clinical features: more indolent; may manifest w/ disorders of tubular function (polyuria from impaired concentrating ability (DI), defective PT reabsorption (features of Fanconi’s syndrome (glycosuria, phosphaturia, aminoaciduria, hypokalemia, and type II renal tubular acidosis [RTA] from bicarbonaturia)), or NAGMA and hyperkalemia (type IV RTA) due to impaired ammoniagenesis, as well as progressive azotemia (rising creatinine and BUN))
        often modest proteinuria (rarely >2 g/d) attributable to decr tubular reabsorption of filtered prs; nephrotic-range albuminuria may occur in some conditions due to development of FSGS
      - sono: may reveal changes of “medical renal disease,” such as incr echogenicity of renal parenchyma w/ loss of corticomedullary differentiation, prominence of renal pyramids, and cortical scarring in some conditions.
      - predominant pathology in chronic TIN: interstitial fibrosis w/ patchy mononuclear cell infiltration and widespread tubular atrophy, luminal dilation, and thickening of tubular basement membranes.
        nonspecific nature of histopathology--> biopsy specimens rarely provide a specific diagnosis--> diagnosis relies on careful analysis of Hx, drug or toxin exposure, associated symptoms, and imaging studies