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(Tubulointerstitial Diseases of the Kidney (ACUTE INTERSTITIAL NEPHRITIS:…

- - - - ARF may occur when crystals deposited in tubular cells and interstitium or when they obstruct tubules.
      - Oliguric ARF, often accompanied by flank pain from tubular obstruction, may occur in patients treated w/ sulfadiazine for toxoplasmosis, indinavir and atazanavir for HIV, and IV acyclovir for severe herpesvirus infections; adverse effect reversible with saline volume repletion and drug withdrawal.
      - [Acute tubular obstruction also the cause of oliguric renal failure in pxs w/] acute urate nephropathy. typically results from severe hyperuricemia from tumor lysis syndrome in patients with lympho- or myeloproliferative disorders treated with cytotoxic agents, but also may occur spontaneously before the treatment has been initiated
      - Prophylactic allopurinol [reduces risk of uric acid nephropathy but is of no benefit once tumor lysis has occurred]
      - [increase tubular flow and] solubility of uric acid w/ alkaline diuresis may be of some benefit; however, emergent treatment with hemodialysis [or rasburicase, a recombinant urate oxidase, is usually required to rapidly lower uric acid levels and restore renal function]
    - - often a diagnosis of exclusion (Sjögren’s syndrome, Behçet’s disease, sarcoidosis, and SLE)
        [Clinical symptoms self-limited in children, but are more apt to follow a relapsing course in adults. renal and ocular manifestations generally respond well to] oral glucocorticoids
      - Additional extrarenal features: fever, anorexia, weight loss, abdominal pain, and arthralgia.
        elevated creatinine, sterile pyuria, mild proteinuria, features of Fanconi’s syndrome, and elevated ESR
      - a systemic AI disease; affects females three times more, median age of onset of 15 years. [hallmark feature: a lymphocyte-predominant interstitial nephritis + a painful anterior uveitis, often bilateral and accompanied by blurred vision and photophobia]
    - - systemic AI primarily targets exocrine glands, esp lacrimal and salivary glands,--> symptoms, such as dry eyes and mouth, that constitute the “sicca syndrome”
      - [Tubulointerstitial nephritis w/ a predominant lymphocytic infiltrate is most common renal manifestation of Sjögren’s syndrome and can be a. w/] distal RTA, nephrogenic DI, and moderate renal failure
      - Diagnosis: positive serologic testing for anti-Ro (SS-A) and anti-La (SS-B) antibodies. many have polyclonal hypergammaglobulinemia.
      - Treatment: initially w/ glucocorticoids, although patients may require maintenance therapy with azathioprine or mycophenolate mofetil to prevent relapse
    - - 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
      - Treatment:
        Discontinuation of offending agent often leads to reversal of the renal injury; may not be completely reversible.
        Glucocorticoid therapy may accelerate renal recovery, but does not appear to impact **long-term renal survival. best reserved for cases w/ severe renal failure in which dialysis is imminent or if renal function continues to deteriorate despite stopping** the offending drug
  - - - used for bipolar treatment; may have several renal sequelae, most common of which is nephrogenic DI
      - renal biopsy: interstitial fibrosis [ and tubular atrophy out of proportion to degree of glomerulosclerosis or vascular disease,
      - Some patients develop more severe proteinuria due to secondary FSGS
    - - long-term use of compound analgesic preparations containing phenacetin [aspirin, and caffeine]
      - classic form: [renal insufficiency,] papillary necrosis, [and a radiographic constellation of small, scarred kidneys with] papillary calcifications in computed tomography
        Shedding of a sloughed necrotic papilla--> gross hematuria + ureteric colic due to ureteral obstruction
    - - stems from abnormal retrograde urine flow from the bladder into one or both ureters and kidneys because of mislocated and incompetent ureterovesical valves
      - high-P sterile reflux--> may impair normal growth of kidneys, when coupled w/ recurrent UTIs in early childhood--> patchy interstitial scarring and tubular atrophy. Loss of functioning nephrons--> hypertrophy of remnant glomeruli--> eventual secondary FSGS.
      - often goes unnoticed until early adulthood when CKD detected. Affected adults are frequently asymptomatic, but may give a hx of prolonged bed-wetting or recurrent UTIs during childhood, and exhibit variable renal insufficiency, hypertension, mild to moderate proteinuria, and unremarkable urine sediment.
      - When both kidneys affected--> progresses inexorably to ESRD; A single affected kidney may go undetected, except for presence of HTN. Renal ultrasound in adults characteristically shows asymmetric small kidneys with irregular outlines, thinned cortices, and regions of compensatory hypertrophy
  - - - 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
  - - - gouty nephropathy (very uncommon nowadays): presence of crystalline deposits of uric acid + monosodium urate salts in the kidney parenchyma--> intrarenal obstruction + infl response
      - hyperuricemia is an independent RF for development of CKD, perhaps through endothelial damage
      - Treatment w/ allopurinol and urine alkalinization effective in preventing uric acid nephrolithiasis