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Tubular lesions

Kidney urine IgA nephropathy Mouse model (Blab/c and hyper IgA vs control) MALDI-QIT-TOF MS LC-LTQ MS Specific lipid signature in the tubular lesion of hyper-IgA mice (63)... [Pg.298]

Two studies in rats have potential implications for humans. In rats with mild to severe lithium-induced nephropathy, urine TV-acetyl-p-D-glucosaminidase was an early indicator of renal insufficiency (369). Both 6Li and 7Li caused reduced urine concentrating ability and increased urine volume and renal tubular lesions, but 6Li was more nephrotoxic (370). The authors suggested that eliminating 6Li from pharmaceutical products might reduce nephrotoxicity (although 6Li accounts for only about 7% of the lithium in such products). [Pg.145]

Lithium-associated changes in kidney morphology include an acute, reversible, and possibly lithium-specific distal tubular lesion and a chronic, nonspecific, and tubulointerstitial nephritis (379). The differential diagnosis of the latter is extensive, and it is not clear if lithium is causative. Lithium received a brief mention in a review of tubulointerstitial nephritis (379). [Pg.146]

The authors concluded that the most likely cause of renal insufficiency was etherified starch-induced tubulopathy and hypothesized that even low amounts of etherified starch as replacement fluid in plasma exchange can cause renal tubular lesions in patients predisposed for other reasons (such as drugs or renal hypoperfusion) to renal insufficiency. In this context, albumin should be combined with replacement fluids other than etherified starch. [Pg.1290]

Guder WG, Hofman W. Markers for the diagnosis and monitoring of renal tubular lesions. Clin Nephrol 1992 38 (SuppI 1) S3-S7. [Pg.119]

Burrows GD, David B, Kincaid-Smith P. Unique tubular lesion after lithium. Lancet 1978 1 1210. [Pg.746]

GritzkaTL, Trump BF. Renal tubular lesions caused by mercuric chloride electron microscopic observations. Am J Pathol 1968 52 1225-78. [Pg.824]

Proteinuria in childhood, with hypertension, etc., or tubular lesions (clearance studies are invaluable). [Pg.301]

Acidification of urine is affected in renal tubular acidosis. This condition may be due to an inborn error of metabolism or to an acquired tubular lesion. The defect may be related either to the secretion of hydrogen ions or to the diffusion of hydrogen ions into the blood as a result of increased permeability of the distal tubule cell wall to secreted hydrogen ions. Because renal tubular acidosis is primarily a defect in hydrogen ion secretion, the formation of ammonia by tubule cells is not affected. [Pg.133]

Patients with diabetes mellitus have a wide range of glomerular and tubular lesions. Glomerular lesions are more common. Increased glomerular filtration rates in diabetics correlate with increased glomerular and kidney size, and these changes are ascribed to increased levels of growth hormone. The most common... [Pg.141]

There are mainly two types of gold-induced nephropathy, one being immune complex type glomerulonephritis and the other limited to tubular lesions. The latter may be induced by the direct toxic action of gold, and this toxicity seems to be dose dependent. The morphological changes in the tubules usually involve gold inclusions [22,... [Pg.309]

Tubular lesions were found in 78.9% of the studied samples. Different epithelial necrosis is the most common lesion observed (78.9% ) while tubular atrophy had been found in (15.8%) of the studied samples. [Pg.614]

Lithium and only a few other drugs have been reported to cause chronic interstitial nephritis, which is usually a progressive and irreversible lesion (Choudhury and Ahmed 2006 Silva 2004). Several renal tubular lesions have been associated with lithium therapy an impaired ability to concentrate urine (nephrogenic diabetes insipidus) has been seen in up to 87% of patients (Markowitz et al. 2000). Acute... [Pg.121]


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