Proteomic identification of alterations in metabolic enzymes and signaling proteins in hypokalemic nephropathy

• Published in: Proteomics (Weinheim) 2006-04, Vol.6 (7), p.2273-2285
• Main Authors: Thongboonkerd, Visith, Chutipongtanate, Somchai, Kanlaya, Rattiyaporn, Songtawee, Napat, Sinchaikul, Supachok, Parichatikanond, Paisal, Chen, Shui-Tein, Malasit, Prida
• Format: Article
• Language: English
• Subjects: Analytical, structural and metabolic biochemistry; Animals; Biological and medical sciences; Body Weight - genetics; Body Weight - physiology; Electrophoresis, Gel, Two-Dimensional; Fundamental and applied biological sciences. Psychology; Hypokalemia - enzymology; Hypokalemia - genetics; Hypokalemia - pathology; Hypokalemic nephropathy; Kidney; Kidney Diseases - enzymology; Kidney Diseases - genetics; Kidney Diseases - pathology; Male; Mice; Mice, Inbred BALB C; Mice, Mutant Strains; Miscellaneous; Potassium; Potassium, Dietary - administration & dosage; Proteins; Proteome; Reproducibility of Results; Signal Transduction - genetics; Signal Transduction - physiology; Urine
• ISSN: 1615-9853; 1615-9861
• DOI: 10.1002/pmic.200500530

Hypokalemic nephropathy caused by prolonged K+ deficiency is associated with metabolic alkalosis, polydipsia, polyuria, growth retardation, hypertension, and progressive tubulointerstitial injury. Its pathophysiology, however, remains unclear. We performed gel‐based, differential proteomics analysis of kidneys from BALB/c mice fed with high‐normal‐K+ (HNK), low‐normal‐K+ (LNK), or K+‐depleted diet for 8 wk (n = 6 in each group). Plasma K+ levels were 4.62 ± 0.35, 4.46 ± 0.23, and 1.51 ± 0.21 mmol/L for HNK, LNK, and KD mice, respectively (p