Renal Concentrating Defect and Organic Osmolytes

Abstract

Under long-term hyperosmotic conditions, renal cells accumulate organic osmolytes preferentially over inorganic ions, which maintain osmotic balance between the inside and the outside of the cells^{6, 7}. Unlike “perturbing” solutes such as NaCl, KCl and urea, the organic osmolytes have relatively weak inhibitory action or even protective effects on enzymes and various cellular processes¹⁵. Organic osmolytes play an important role in the osmoregulation of the kidney. However, the relationship between renal concentrating defect and organic osmolytes has not been well clarified. In kidney in situ, medullary hypertonicity is constructed by medullary cells themselves. So, delayed or decreased accumulation of osmolytes in the renal medulla may be the cause of renal concentrating defects. In this study, we chose K⁺-depleted rats as a model of renal concentrating defect. In K⁺ depletion, a renal concentrating defect is a prominent and consistent finding. Several defects associated with urinary concentrating ability have been reported, including prostaglandin overproduction⁹, blunted responsiveness to antidiuretic hormone², reduced papillary solute content⁴, abnormal medullary oxidative metabolism^{3, 13}, altered ADH release¹⁰, and primary polydipsia¹. Decreased accumulation of organic osmolytes in renal medulla could explain some of these abnormalities associated with the concentrating defect.