Protein Restriction in Chronic Renal Failure: Correlation between Creatinine Clearance and the Reciprocal Serum Creatinine

Author(s):  
J. B. Rosman ◽  
N. Gretz ◽  
G. K. van der Hem ◽  
M. Strauch ◽  
A. J. M. Donker
1995 ◽  
Vol 6 (5) ◽  
pp. 1379-1385
Author(s):  
J Coresh ◽  
M Walser ◽  
S Hill

Concerns have been raised about the possibility of protein restriction resulting in malnutrition and poor subsequent survival on dialysis. However, no studies have examined patients treated with protein restriction to determine their subsequent survival on dialysis. This study prospectively monitored 67 patients with established chronic renal failure (mean initial serum creatinine of 4.3 mg/dL) who were treated with a very low-protein diet (0.3 g/kg per day) supplemented with either essential amino acids or a ketoacid-amino acid mixture and observed closely for clinical complications. Forty-four patients required dialysis. Once dialysis was started, dietary treatment was no longer prescribed. The cumulative mortality rate during the first 2 yr after starting dialysis was 7% (95% confidence interval, 0 to 16%). During this period, only two deaths occurred compared with 11.5 deaths expected on the basis of national mortality rates adjusted for age, sex, race, and cause of renal disease (P = 0.002). However, the protective effect was limited to the first 2 yr on dialysis. Thereafter, mortality rates increased, resulting in a total of 10 deaths during 96.4 person-years of follow-up, which was not significantly lower than the 14.9 deaths expected (P = 0.25). Extrapolation of sequential serum creatinine measurements made before dietary treatment suggests that the improved survival cannot be due to the early initiation of dialysis. Although the lack of an internal control group and data on dialysis lends uncertainty, the large difference in mortality rate between these patients and the nationwide experience indicates that protein restriction and close clinical monitoring predialysis does not worsen and may substantially improve survival during the first 2 yr on dialysis. These findings point out the importance of studying predialysis treatments as a means for lowering mortality on dialysis.


1981 ◽  
Vol 27 (9) ◽  
pp. 1618-1619 ◽  
Author(s):  
G Digenis ◽  
A G Hadjivassiliou ◽  
D Mayopoulou-Symvoulidis ◽  
N Tsaparas ◽  
A Symvoulidis

1970 ◽  
Vol 7 (1) ◽  
pp. 10-14
Author(s):  
Roksana Yeasmin ◽  
Md Nizamul Hoque Bhuiyan ◽  
Sultana Parveen ◽  
Shamim Ara Ferdous ◽  
Nazmun Nahar

A case control study was done during the period of July 2004 to 2005. The study was carried out in the Department of Biochemistry, Dhaka Medical College, Dhaka. 50 diagnosed chronic renal failure patients of both sexes not yet treated by dialysis and 50 age and sex matched healthy subjects were included in the study as case (Group-II) and control (Group-I) respectively. In this study, mean serum HS CRP concentration of CRF patients (50.938 ±38.88)mg/l found to be significantly elevated in comparison to control (1.12±.29mg/l). In CRF patients, serum HS CRP found to show a strong negative correlation with creatinine clearance and a strong positive correlation with blood urea, serum creatinine. This study shows an inverse linear relationship between HS CRP and CCRin contrast to the inverse curvilinear relationship found to exist between serum creatinine and creatinine clearance. Regression analysis between CCR and HS CRP shows a rise of HS CRP Y one unit (mg/l) is accompanied by creatinine clearance to be decreased by 0 .44ml/min. Mean serum HS CRP concentration in chronic renal failure increases significantly. Early phase of decreased CCR can not be detected by the serum creatinine because serum creatinine does not increase until there is significant fall ( 30 ml/min) of creatinine clearance. In contrast to this serum HS CRP begins to rise from the very beginning of the fall of creatinine clearance. So the early phase of decreased creatinine clearance could be detected by simultaneous rise of serum HS CRP. Key Words: HS CRP, CRF, CCR.     DOI = 10.3329/jom.v7i1.1356 J MEDICINE 2006; 7 : 10-14


1970 ◽  
Vol 1 (1) ◽  
Author(s):  
LI Yang

Objective To study the efficacy and safety of rhubarb aconite decoction combined with acupoint application in the treatment of chronic renal failure (CRF). Methods 106 cases of CRF patients were randomly divided into two groups, the control group of 53 cases of conventional Western medicine treatment, the treatment group of 53 cases of rhubarb aconite combined with acupoint application, 2 groups were treated continuously for 20 d. (UA), blood urea nitrogen (BUN) and endogenous creatinine clearance (Ccr) were measured before and after treatment. The levels of serum creatinine (Cr), serum creatinine (UA), blood urea nitrogen (BUN) and endogenous creatinine clearance (Ccr) were measured and compared. Level, and observe the occurrence of adverse reactions during the two groups of treatment.


Author(s):  
Pusparini .

The Gold standard for the evaluation of the glomerular filtration rate (GFR) is inulin clearance, but in widespread use is prevented by several technical difficulties. The most commonly used marker for GFR is serum creatinine alone or in conjunction with 24 hoururine collection for determination of creatinine clearance, but these marker have several limitation include following: influence of age,sex, muscle mass on endogenous creatinine production, dietary intake and the difficulties of 24 hour urine collection. Fifty six patientwith chronic renal failure and 53 control had analyze for serum creatinin, creatinine clearance and serum cystatin C. The chronic renalfailure patient aged range from (64 + 14.54) year and the control group aged range from (62.5+ 17.5) year. The proposed of this studywas to compare cystatin C with another parameter for renal function test. The result showed that in control group serum creatinineand creatinine clearance had influence with age, sex and body mass index, but serum cystatin C was not. The normal value of cystatinC was (0.85 + 0.13) mg/dL In chronic renal failure group there were significant correlation between level of cystatin C with creatininclearance (p = 0.000, r = 0.69). The level of cystatin C increase higher than serum creatinine in patient with low clearance creatinine.In control group we were determined low creatinine clearance in patient with normal serum creatinine and cystatin C.


1998 ◽  
Vol 275 (1) ◽  
pp. F154-F163 ◽  
Author(s):  
Michael G. Stockelman ◽  
John N. Lorenz ◽  
Frost N. Smith ◽  
Gregory P. Boivin ◽  
Amrik Sahota ◽  
...  

In humans, adenine phosphoribosyltransferase (APRT, EC 2.4.2.7 ) deficiency can manifest as nephrolithiasis, interstitial nephritis, and chronic renal failure. APRT catalyzes synthesis of AMP from adenine and 5-phosphoribosyl-1-pyrophosphate. In the absence of APRT, 2,8-dihydroxyadenine (DHA) is produced from adenine by xanthine dehydrogenase (XDH) and can precipitate in the renal interstitium, resulting in kidney disease. Treatment with allopurinol controls formation of DHA stones by inhibiting XDH activity. Kidney disease in APRT-deficient mice resembles that seen in humans. By age 12 wk, APRT-deficient male mice are, on average, mildly anemic and smaller than normal males. They have extensive renal interstitial damage (assessed by image analysis) and elevated blood urea nitrogen (BUN), and their creatinine clearance rates, which measure excretion of infused creatinine as an estimate of glomerular filtration rate (GFR), are about half that of wild-type males. APRT-deficient males treated with allopurinol in the drinking water had normal BUN and less extensive visible renal damage, but creatinine clearance remained low. Throughout their lifespans, homozygous null female mice manifested significantly less renal damage than homozygous null males of the same age. APRT-deficient females showed no significant impairment of GFR at age 12 wk. Consequences of APRT deficiency in male mice are more pronounced than in females, possibly due to differences in rates of adenine or DHA synthesis or to sex-determined responses of the kidneys.


The Lancet ◽  
1985 ◽  
Vol 325 (8426) ◽  
pp. 465-466 ◽  
Author(s):  
H.A. Bock ◽  
F.P. Brunner ◽  
JohanB. Rosman ◽  
WimJ. Sluiter ◽  
AbJ.M. Donker

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