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Tubularinterstitial Nephritis
Karthik Ranganna, MD, is an assistant professor of medicine at Drexel University College of medicine, and a staff nephrologist at Hahnemann University Hospital in Philadelphia. Alan B. Schwartz, MD, is a professor of medicine in the division of nephrology and hypertension at Drexel University College of Medicine where he is also director of continuing medical education. Here, they define tubulointerstitial disease, discuss the clinical features and the etiologic causes of both acute and chronic versions of the disease, and discuss a variety of associated neuropathies and myelomas. Tubulointerstitial nephritis is defined as kidney disease involving the tubules and the interstitium. The authors note that 15 – 20% of acute renal failure is due to acute tubular interstitial disease, and 20 to 30% of chronic tubulointerstitial cases progress to end-stage renal disease. Precipitating factors for tubulointerstitial disease include metabolic, immunologic and neoplastic disorders, as well as exposure to environmental agents or to medications. The best predictor of outcome in renal disease, the authors contend, is the degree of tubulointerstitial damage seen in the renal biopsy; the greater the damage, the poorer the outcome. Drs Ranganna and Schwartz go on to discuss the gross and histologic findings in acute and chronic tubulointerstitial disease, and note the clinical features of both the acute and chronic forms. In the acute form, onset is over two to 40 days. In the chronic form, patients generally present with gradually increasing blood urea nitrogen and creatinine, and difficult to control blood pressure. Clinical features include damage to the proximal tubule, natriuresis, bicarbonaturia, uricosuria, and aminoaciduria (Franconi-like syndrome). Chronic tubulointerstitial disease can be the result of chronic exposure to non-steroid anti-inflammatory drugs (NSAIDs) and immunosuppressive agents such as cyclosporine, tacrolimus, and lithium. Other causes of interstitial disease include cystic disorders of the kidneys, hematologic disorders like plasma cell dyscrasias, and sickle cell hemoglobinopathies. Doctors Ranganna and Schwartz discuss antibiotic-induced ATN and its manifestations, and go on to explain the physiology and pathogenesis of analgesic nephropathy. The lecture continues with a discussion of lithium-induced kidney disease, Chinese herbal nephropathy, cadmium nephropathy, acute uric acid nephropathy and hypercalcemia nephropathy. The authors conclude with a discussion of the association between interstitial kidney disease and multiple myeloma. Management of myeloma kidney may include plasmapheresis which, say the authors, has had varying degrees of success. More than 30 illustrations accompany this lecture. |
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