Kidney disease, chronic serum creatinine

A 73-year-old man with a history of diabetes mellitus, chronic kidney disease, gout, osteoarthritis, and hypertension is hospitalized with possible urosepsis. He recently completed a 10-day course of antibiotics and was ready for discharge when his morning labs showed an increase in BUN and serum creatinine concentration. Upon examination, he was found to have 2+ pitting edema, weight gain, nausea, elevated blood pressure, and rales on chest auscultation. 

A 55-year-old woman with polycystic kidney disease and chronic renal impairment (serum creatinine concentration 181 pmol/l) received gadodiamide (Omniscan) for cerebral angiography there were no adverse effects and the serum creatinine was unchanged. (27)... 

Levey AS, Coresh J,GreeneT, Marsh J, Stevens LA, KusekJW,Van Lente F, for Chronic Kidney Disease EpidemioiogyCoiiaboration. Expressing the Modificationof Diet in Renai Disease Study Equation for Estimating Giomeruiar Fiitration Rate with Standardized Serum Creatinine Vaiues Ciinicai Chemistry 2007 53 766-772. 

In a large prospective population sample, primarily a cancer research project (CLUE study), Haroun [42] noted that smoking accounted for no less than 30% of the "attributable risk" of chronic kidney disease (CKD), defined as serum creatinine > 2 mg/ dl, and this was particularly true in the elderly. 

Bostom AG, Kronenberg F, Ritz E. Predictive performance of renal function equations for patients with chronic kidney disease and normal serum creatinine levels. J Am Soc Nephrol 2002 13 2140-4. 

ACE inhibitors are well tolerated in most patients but are not absent of side effects. ACE inhibitors decrease aldosterone and can increase potassium serum concentrations. Usually the increase in potassium is small, but hyperkalemia is possible. It is seen primarily in patients with chronic kidney disease or diabetes mellitus and in those on concomitant ARBs, nonsteroidal anti-inflammatory drugs, potassium supplements, or potassium-sparing diuretics. Judicious monitoring of potassium and serum creatinine values within 4 weeks of starting or increasing the dose of an ACE inhibitor often can identify these abnormalities before they evolve into more serious complications. 

Newer markers that identify patients at high risk of mortality or reinfarction that are under development but have not been incorporated currently into routine patient care include C-reactive protein, a maker of vascular inflammation elevated serum creatinine or reduced creatinine clearance, identifying patients with chronic kidney disease and brain (B-type) natriuretic peptide (BNP), which is released predominately from ventricular myocytes in response to cell stretch as the infarct remodels. Dialysis patients have a 1-year mortality rate of more than 40% following a first MI. ... 

Renal blood flow and GFR decline progressively with age. Progressive sclerosis of glomemh occurs, and residual glomerular and tubular units increase function in compensation, similarly to patients with chronic kidney disease. This decline in renal function is not accompanied by a rise in the serum creatinine concentration due to the age-related decline in muscle mass and decreased creatinine generation. Older individuals are also more likely to have heart failure and hepatic insufficiency, which also reduce renal hlood flow. Together, these processes predispose the elderly to an increased risk of nephrotoxicity. ... 

Taiwanese chronic kidney disease patients N = 108) without diabetes Body Pb measured by chelation mobilization <80 pg Patients randomly assigned to EDTA chelation control groups chelated 3 months, then 24 months periodically patients followed to 1.25 times baseline serum creatinine and with changes in GFR Patients without chelation showed increase in serum creatinine over baseline (N= 14) and/or mean decrease in GFR of 4.6 ml/min/1.73 m Lin et al. (2006)... 

The very low mean PbBs in these women and those men and women in the Muntner et al. (2003) U.S. NHANES III provided good evidence that the relative threshold for Pb nephrotoxic effects with environmental exposures in the general population is an order of magnitude less than was observed in the older occupational Pb literature, 60 pg/dl. Low body lead burdens indexed as chelatable Pb amounts of <80 pg/dl were also found to be a predictor of decreased kidney function (Lin et al., 2006). Taiwanese chronic kidney disease patients (N = 108) without diabetes were assigned to chelation and nonchelation groups. Those patients who were not periodically chelated over a 24-month testing period sustained a mean reduction in GFR of 4.6 ml/min/1.732 m and showed increased serum creatinine. 

Epoetin delta differs from the other erythropoietin derivatives in that it is produced in a human cell line using gene-activation technology. It has been approved in Europe but not in the USA for the treatment of anemia associated with chronic kidney disease. In patients with cancer and anemia who were given epoetin delta, possible treatment-related serious adverse events were hypertension, increased serum creatinine, and peripheral vascular disease [99 ]. There was a correlation with higher doses, suggesting that a dose of 150 lU/kg would be most appropriate to start with for this indication. 

In addition to an increase in serum urea and creatinine levels, uric acid and inorganic phosphate levels also increase in chronic renal failure. The increase in serum inorganic phosphate leads to deposition of calcium phosphate in bones, causing hypocalcemia. In the early stages of chronic renal failure, calcium levels are restored by the stimulation of parathyroid hormone. However, as the renal disease progresses, the ability of the kidney to hydroxylate vitamin D and thus convert it to the active form decreases, thereby affecting the uptake of calcium by the gut and thus perpetuating hypocalcemia. Serum alkaline phosphatase levels increase due to disordered bone metabolism. Loss of bicarbonate is seen in some patients with increased parathyroid hormone activity. 

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