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post in: Lifestyle, Health Date:25 Oct 2017, 06:54 views:4313
A normal kidney contains approximately 1 million nephrons, each of which contributes to the total glomerular over filtration rate (GFR).
In the face of renal injury (regardless of the etiology the kidney has an innate ability to maintain GFR, despite progressive destruction of nephrons, as the remaining healthy nephrons manifest hyperfiltration and compensatory hypertrophy. This nephron adaptability allows for continued normal clearance of plasma solutes. Plasma levels of substances such as urea and creatinine start to show measurable increases only after total GFR has decreased.
The plasma creatinine value will approximately double with a 50 reduction in GFR. For example, a rise in plasma creatinine from a baseline value.6 mg/dL.2 mg/dL in a patient, although still within the adult reference range, actually represents a loss of 50 of functioning nephron mass.
The hyperfiltration and hypertrophy of residual nephrons, although beneficial for the reasons noted, has been hypothesized to represent a major cause of progressive renal dysfunction.
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). Factors other than the underlying disease process and glomerular hypertension that may cause progressive renal injury include the following: Systemic hypertension, nephrotoxins (eg, nonsteroidal anti-inflammatory drugs nsaids, intravenous contrast media).
Decreased perfusion (eg, from severe dehydration or episodes of shock). Proteinuria (in addition to being a marker of CKD).
Hyperlipidemia, hyperphosphatemia with calcium phosphate deposition, smoking.
Uncontrolled diabetes, thaker et al found a strong association between episodes of acute kidney injury (AKI) and cumulative risk for the development of advanced CKD in multiple hospitalized patients with diabetes mellitus. 7, any AKI versus no AKI was a risk factor for stage 4 CKD, and each additional AKI episode doubled that risk. 7, findings from the Atherosclerosis Risk in Communities (aric) Study, a prospective observational cohort, suggest that inflammation and hemostasis are antecedent pathways for CKD.
8, this asthma study used data from 1787 cases of CKD that developed between 19Childhood renal function and CKD in children.