Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032617 (polyuria)
 3,056 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tubulointerstitial nephritis developed in 25 of 34 (74%) rabbits challenged intravenously for 2-20 weeks with adjuvant and endotoxin free homologous Tamm-Horsfall protein (THP). Lesions were characterized by focal mononuclear cellular infiltrates and microscopic scarring localized to distal nephron segments identified as thick ascending limb of the loop of Henle. Interstitial deposits of THP were found in the kidneys of more severely affected rabbits and metabolic studies demonstrated transient polyuria and tubular dysfunction. Elevations in serum IgG antibody against THP were detected in seven of 34 challenged rabbits. Tubulointerstitial nephritis was found in six of the seven rabbits with elevated antibody as well as in 19 of 27 rabbits without elevated antibody. By contrast, peripheral lymphocytes from eight of 13 rabbits with tubulointerstitial nephritis were cytotoxic against target fibroblasts in the presence of THP as compared to none of eight age matched challenged or unchallenged rabbits with normal kidneys. The presence or absence of endotoxin in vitro did not influence determinations of antibody- or lymphocyte-mediated cytotoxicity. These observations suggest that the tubulointerstitial nephritis which develops in rabbits challenged with THP is primarily the result of cell-mediated immune responses directed against THP, and does not require the presence of endotoxin in the challenge solution, or serum IgG antibodies directed against THP.
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PMID:Tubulointerstitial nephritis in rabbits challenged with homologous Tamm-Horsfall protein: the role of endotoxin. 661 57

Tubulointerstitial nephritis is a common clinicopathological finding in leptospirosis. Clinically, nonoliguric acute kidney injury (AKI), hypokalemia, sodium, and magnesium wasting frequently occur in leptospirosis. The exact mechanisms of renal involvement remain largely unclear. Immunohistochemistry to detect expression of the endogenous sodium/hydrogen exchanger isoform 3 (NHE 3), aquaporin 1 and 2, alpha-Na(+)K(+)ATPase, and sodium-potassium-chloride cotransporter in its NKCC2 isoform was performed on kidneys removed during autopsy of human leptospirosis cases and kidneys removed during autopsy of human non-leptospirosis cases with and without evidence of acute tubular necrosis (ATN). A decrease in NHE 3, aquaporin 1, and alpha-Na(+)K(+)ATPase expression occurred in proximal convoluted tubule cells. Expression of aquaporin 1 was preserved along the descending thin limb of the loop of Henle in the outer medulla. alpha-Na(+)K(+)ATpase expression was essentially preserved in the distal tubules, i.e., the thick ascending limb of the loop of Henle, macula densa, and distal convoluted tubule. Aquaporin 2 expression in the collecting tubules was enhanced compared to those of non-leptospirotic kidneys. NKCC2 cotransport isoform was expressed in the thick ascending limb of the loop of Henle and was essentially preserved in leptospirotic kidneys. Primary injury of the proximal convoluted tubules is regarded as the hallmark of the kidney in leptospirosis. Sodium and water transport are particularly affected with increased distal potassium excretion, hypokalemia, and polyuria. Enhanced expression of aquaporin 2 in medullary collecting tubules is probably an attempt to retain water during the nonoliguric phase of renal failure.
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PMID:Acute kidney injury in human leptospirosis: an immunohistochemical study with pathophysiological correlation. 2021 29