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These anatomic and functional changes in renal vasculature appear to contribute to an age-related decrease in renal blood flow.

Aspects of pediatric kidney function and the measure of creatinine are informative not only for children but also for adults.

For example, it is important to realize that creatinine is derived from muscle and, therefore, that children and smaller individuals have lower creatinine levels independent of the GFR.

The increased glomerular capillary pressure may damage the capillaries, leading initially to secondary focal and segmental glomerulosclerosis (FSGS) and eventually to global glomerulosclerosis.

This hypothesis is supported by studies of five-sixths nephrectomized rats, which develop lesions identical to those observed in humans with chronic kidney disease (CKD).

Plasma levels of substances such as urea and creatinine start to show measurable increases only after total GFR has decreased to 50%.

The plasma creatinine value will approximately double with a 50% reduction in GFR.

Fortunately, CKD during childhood is rare and is usually the result of congenital defects, such as posterior urethral valves or dysplastic kidney malformations. Genetic kidney diseases are also frequently manifested in childhood CKD.

Advances in pediatric nephrology have enabled great leaps in survival for pediatric CKD and end-stage renal disease (ESRD), including for children who need dialysis or transplantation.

The GFR peaks during the third decade of life at approximately 120 m L/min/1.73 m Ischemic obsolescence of cortical glomeruli is predominant, with relative sparing of the renal medulla.

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