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There are four main causes of chronic tubulointerstitial disease These are discussed below Other causes include multiple myeloma and gout, which are discussed in the section on multisystem disease with variable kidney involvement (below)
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B Vesicoureteral Reflux
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Reflux nephropathy is primarily a disorder of childhood and occurs when urine passes retrograde from the bladder to the kidneys during voiding It is the second most common cause of chronic tubulointerstitial disease It occurs as a result of an incompetent vesicoureteral sphincter Urine can extravasate into the interstitium; an inflammatory response develops, and fibrosis occurs The inflammatory response is due to either bacteria or normal urinary components
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A Obstructive Uropathy
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The most common cause of chronic tubulointerstitial disease is prolonged obstruction of the urinary tract In
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Patients are adolescents or young adults with hypertension, renal insufficiency, and a history of urinary tract infections as a child Focal glomerulosclerosis is often seen This is a cause of substantial proteinuria, unusual in most tubular diseases Renal ultrasound or IVP can show renal scarring and hydronephrosis Although most damage occurs before age 5 years, progressive renal deterioration to ESRD continues as a result of the early insults
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Polyuria is common because tubular damage leads to inability to concentrate the urine Dehydration can also occur as a result of a salt-wasting defect in some individuals
B Laboratory Findings
Patients are hyperkalemic because the distal tubules become aldosterone resistant A hyperchloremic renal tubular acidosis is characteristic The cause of the renal tubular acidosis is threefold: (1) reduced ammonia production, (2) inability to acidify the distal tubules, and (3) proximal tubular bicarbonate wasting The urinalysis is nonspecific, as opposed to that seen in acute interstitial nephritis Proteinuria is typically less than 2 g/d (owing to inability of the proximal tubule to reabsorb freely filterable proteins); a few cells may be seen; and broad waxy casts are often present
C Analgesics
Analgesic nephropathy is most commonly seen in patients who ingest large quantities of analgesic combinations The drugs of concern are phenacetin, paracetamol, aspirin, and NSAIDs Chronic ingestion of 1 g/d for 3 years is the typical amount needed for renal dysfunction This disorder occurs most frequently in individuals who are using analgesics for chronic headaches, muscular pains, and arthritis Most patients grossly underestimate their analgesic use Tubulointerstitial inflammation and papillary necrosis are seen on pathologic examination Papillary tip and inner medullary concentrations of some analgesics are tenfold higher than in the renal cortex Phenacetin once a common cause of this disorder and now rarely available is metabolized in the papillae by the prostaglandin hydroperoxidase pathway to reactive intermediates that bind covalently to interstitial cell macromolecules, causing necrosis Aspirin and other NSAIDs may worsen the damage by decreasing medullary blood flow (via inhibition of prostaglandin synthesis) and decreasing glutathione levels (which are necessary for detoxification) Patients can exhibit hematuria, mild proteinuria, polyuria (from tubular damage), anemia (from gastrointestinal bleeding), and sterile pyuria As a result of papillary necrosis, sloughed papillae can be found in the urine An IVP may be helpful for detecting these contrast will fill the area of the sloughed papillae, leaving a ring shadow sign at the papillary tip
Treatment
Treatment depends first upon identifying the disorder responsible for renal dysfunction The degree of interstitial fibrosis that has developed can help predict recovery of renal function Once there is evidence for loss of parenchyma (small shrunken kidneys or interstitial fibrosis on biopsy), nothing can prevent the progression toward ESRD Treatment is then directed at medical management Tubular dysfunction may require potassium and phosphorus restriction and sodium, calcium, or bicarbonate supplements If hydronephrosis is present, relief of obstruction should be accomplished promptly Prolonged obstruction leads to further tubular damage particularly in the distal nephron which may be irreversible despite relief of obstruction Neither surgical correction of reflux nor medical therapy with antibiotics can prevent deterioration toward ESRD once renal scarring has occurred Patients in whom lead nephropathy is suspected should continue chelation therapy with EDTA if there is no evidence of irreversible renal damage (eg, renal scarring or small kidneys) Continued exposure should be avoided Treatment of analgesic nephropathy requires withdrawal of all analgesics Stabilization or improvement of renal function may occur if significant interstitial fibrosis is not present Hydration during exposure to analgesics may also have some beneficial effects
Harris DC Tubulointerstitial renal disease Curr Opin Nephrol Hypertens 2001 May;10(3):303 13 [PMID: 11342791] Huerta C et al Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population Am J Kidney Dis 2005 Mar;45(3):531 9 [PMID: 15754275] Kodner CM et al Diagnosis and management of acute interstitial nephritis Am Fam Physician 2003 Jun 15;67(12):2527 34 [PMID: 12825841]
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