Effects of long-term dehydration and quick rehydration on the camel kidney: pathological changes and modulation of the expression of solute carrier proteins and aquaporins

Abstract The kidney of the one-humped camel has a remarkable capacity to preserve water and solute during extremes of long-term dehydration. We investigated the effects of dehydration and subsequent rehydration on camel kidney morphology at the ultrastructural level and the expression of aquaporins and solute carrier proteins. In light microscopy, dehydration induced few degenerative and necrotic changes in cells of the cortical tubules with little effect on medullary cells. Ultrastructural changes were mainly observed in some of the glomerular and tubular cells with insignificant changes in the collecting ducts of medulla. These changes included condensation of nuclear chromatin, vacuolization of cytoplasm, swelling of mitochondria, degradation or loss of brush borders of proximal tubules, cracking of major processes of some podocytes and degeneration of lysosomes and endoplasmic reticulum. Cell death, apoptotic-like bodies and changes in the basolateral membranes were infrequent and nephrolithiasis was not detected. Chronic nephropathy, mainly interstitial fibrosis and glomerular sclerosis induced by recurrent dehydration in human and animal models were not observed. Modulation of SLC proteins, AQP 1, 2, 3, 4, 9 and regulation of gene mRNAs expression levels during dehydration/rehydration play important role in water conservation and cell protection favoring kidney cellular restoration to near normal.