Corticomedullary junction

Equivalent to 108 mg Ni/kg BW daily for 180 days as nickel sulfate Drinking water Renal tubular damage at the corticomedullary junction 6... 

After peroral intake of nickel sulphate in mice, kidney damage appeared at the corticomedullary junction [296]. There was loss of renal tubular epithelial cells and protein loss, giving numerous hyaline casts in the renal tubules and collecting ducts, especially prominent in the renal papillae. 

The kidney begins to function as soon as there are functional nephrons at the corticomedullary junction. Nephron development continues during this time in the periphery of the cortex. Production of urine starts at about the end of the 3rd month in humans and by gestation day 17 or 18 in rats. Urine production is not necessary for waste excretion from the fetus, as this is taken care of by the placenta. Urine production is necessary to maintain proper amniotic fluid volume. Fetuses without kidneys or with insufficient urine production have oligohydramnios, too little amniotic fluid. Oligohydramnios can lead to abnormal development by physically confining the fetus, sometimes resulting in amputation or deformation of limbs in utero. 

Acute exposure to unleaded gasoline and a variety of light hydrocarbons present in gasoline produces a nephropathy in male rats characterized by (1) an excessive accumulation of protein (hyaline droplets) in epithelial cells of proximal tubule, (2) accumulation of casts at the corticomedullary junction, and (3) evidence of mild tubular regeneration. This nephropathy only occurs in male rats female rats and mice do not show any renal pathology. A number of chemicals present in unleaded petrol when tested alone have been shown to produce nephropathy and, in particular 2,2,4-trimethylpentane and decalin have been used as model compounds. Certain other industrial chemicals (1,4-dichlorobenzene and isophorone), natural products (o-limonene), and pharmaceuticals (levamisole) also produce this male-rat-specific nephropathy. Chronic exposure of male rats to unleaded petrol, 1,4-dichlorobenzene, isophorone, or o-limonene ultimately leads to the induction of a low incidence of renal adenomas and carcinomas. 

Lesions were prominent at the corticomedullary junction where abrasion of the brush border of the tubular epithelium and desquamation of tubular epithelial cells were commonly seen. This tubular injury was associated with increased blood urea nitrogen levels and enhanced urinary excretion of endopeptidase 24.11 [156], an enzyme of the brush border of the proximal tubular epithehum. 

This disease group is defined by renal cysts at the corticomedullary junction and classified into a recessive form (nephronophthisis) and dominant form (medullary cystic kidney disease) (OMIM 256100 and 174000). Nephronophthisis is genetically heterogeneous, four genes have been mapped and identified (NPHPl-4). Additional genes can be expected. 

The varying responses of experimental NC reflect the complex and multifactorial etiology of NC best. There are two distinct forms of experimental NC in rats diffuse, but predominantly corticomedullary following sodium phosphate, and predominantly cortical following calcium glucomide (Four man 1959). Phosphate-induced NC in rabbits occurs maximally at the corticomedullary junction, but also frequently in the cortex, seldom in the medulla. NC was not permanent or stable, but improved on return to a normal diet (Cramer et al. 1998b). 

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