Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The leukocyte Na/H antiporter has been studied in patients with end-stage renal failure on maintenance haemodialysis. Thirteen non-diabetic haemodialysis patients (CRF group) and eight haemodialysis patients with diabetic nephropathy (CRF-DM group) were investigated. Measurements were made using the pH-sensitive fluorescent dye bis (carboxyethyl) carboxyfluorescein (BCECF). The initial intracellular pH (pHi), intracellular buffering capacity, and Na/H antiporter Vmax (at pHi = 6.0) have been recorded in bicarbonate-free solutions. The mean initial intracellular pH in the CRF group was 7.34 (SD 0.05, P less than 0.004) and this was significantly less than the CRF-DM group (7.42, SD 0.07) and normal controls (7.43, SD 0.09, n = 25). The mean intracellular buffering capacity was normal in the CRF and CRF-DM groups. The mean Na/H antiporter Vmax was also normal in the CRF and CRF-DM groups (56.5, SD 9.9; and 56.8, SD 12.8, mmol/l per min respectively compared to 55.2, SD 8.8, mmol/l per min in controls). These data are discussed with reference to the reported high values of Na/H antiporter Vmax in diabetic patients with early nephropathy. This abnormality does not appear to be present in end-stage diabetic nephropathy.
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PMID:Leukocyte intracellular pH and Na/H antiporter activity in uraemia and type I diabetes mellitus. 132 83

This study investigated the effect of chronic hypertonicity on the OKP cell Na/H antiporter, encoded by Na/H exchanger 3 (NHE3). Chronic (48 h) increases in extracellular glucose, mannitol, or raffinose concentration caused a significant increase in Na/H antiporter activity, while increases in urea concentration were without effect. This effect was seen with changes in osmolality of only 20 mOsm/liter, a magnitude that is observed clinically in poorly controlled diabetes mellitus. Increases in mannitol concentration acutely inhibited and chronically stimulated Na/H antiporter activity. The increase in Na/H antiporter activity induced by hypertonic incubation was resistant to 10(-7) and 5 x 10(-6) M but inhibited by 10(-4) M ethylisopropyl amiloride, consistent with regulation of NHE3. In addition, hypertonicity increased total cellular and plasma membrane NHE3 protein abundance twofold, with only a small increase in NHE3 mRNA abundance. We conclude that chronic pathophysiologically relevant increases in tonicity lead to increases in NHE3 protein abundance and activity. This may be responsible for increased proximal tubule apical membrane Na/H antiporter activity in poorly controlled diabetes mellitus, which could then contribute to hypertension, glomerular hyperfiltration and diabetic nephropathy.
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PMID:Chronic hyperosmolality increases NHE3 activity in OKP cells. 942 79