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The end results of reflux nephropathy can include high blood pressure, excessive protein loss in the urine, and eventually kidney failure. When reflux nephropathy is suspected as a cause of kidney disease, other conditions to consider include chronic pyelonephritis , obstructive uropathy , and analgesic overuse.
Scarring disturbs the filtering process of the kidneys and allows protein to leak from the blood into the urine. However, glomerulosclerosis is one of many causes of proteinuria. A kidney biopsy (the removal of a tiny part of the kidney with a needle) may be necessary to determine whether a patient has glomerulosclerosis or another kidney problem.
Most children with vesicoureteral reflux are asymptomatic. Vesicoureteral reflux may be diagnosed as a result of further evaluation of dilation of the kidney or ureters draining urine from the kidney while in utero as well as when a sibling has VUR (though routine testing in either circumstance is controversial).
The length of peritoneal dialysis treatment appears to be the primary risk factor for encapsulating peritoneal sclerosis development. The incidence of encapsulating peritoneal sclerosis rose with the length of peritoneal dialysis (PD) in an Australian survey; for patients on PD for more than 2, 5, 6, and 8 years, the rates were 1.9, 6.4, 10.8 ...
Excessive ADH causes an inappropriate increase in the reabsorption in the kidneys of solute-free water ("free water"): excess water moves from the distal convoluted tubules (DCTs) and collecting tubules of the nephrons – via activation of aquaporins, the site of the ADH receptors – back into the circulation. This has two consequences.
Neurological examination is usually normal. Misdiagnosis as benign infantile spasms or epileptic seizures is common, particularly where clear signs or symptoms of gastro-oesophageal reflux are not apparent. Early diagnosis is critical, as treatment is simple and leads to prompt resolution of the movement disorder. [2]
Indication for kidney biopsy remains unclear as histologic findings do no reveal the cause of congenital nephrotic syndrome, but findings may help in developing treatment strategies. [1] [2] Findings on light microscopy can vary from minimal change nephropathy to focal segmental glomerulosclerosis or diffuse mesangial sclerosis.
Treatment of secondary membranous nephropathy is guided by the treatment of the original disease. For treatment of idiopathic membranous nephropathy, the treatment options include immunosuppressive drugs and non-specific anti-proteinuric measures such as ACE inhibitors or angiotensin II receptor blockers .
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