Chronic progressive renal disease: Rate of change of serum creatinine concentration

Rutherford, W. E.; Blondin, Joan; Miller, John P.; Greenwalt, A; Vavra, John D.

doi:10.1038/ki.1977.8

Cited by 217 publications

(55 citation statements)

References 18 publications

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“…In previous studies in smaller numbers of participants, a linear rate of decline has been reported (23)(24)(25)(26). In this large cohort, we found that as renal function declined, the rate of decline of renal function accelerated.…”

Section: Discussionsupporting

confidence: 55%

A Comparison of Iothalamate-GFR and Serum Creatinine-Based Outcomes

Lewis¹,

Greene²,

Appel³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. In renal clinical trials, both slope-based and timeto-event renal outcomes have been used. These outcomes are typically based on estimates of GFR obtained using creatinine or iothalamate GFR (iGFR). The African American Study of Kidney Disease and Hypertension (AASK) was a trial in 1094 African Americans with hypertensive nephrosclerosis, which examined the effects of two levels of BP control and three antihypertensive regimens. This study compared the effects of the AASK interventions on outcomes based on serum creatinine with corresponding outcomes based on iGFR using 9742 matched pairs of iGFR and serum creatinine measurements. The iGFR-based outcomes included (1) a time-to-event composite outcome including a 50% GFR decline, ESRD, or death; (2) a composite outcome including a 50% GFR decline or ESRD; (3) mean decline in GFR in the first 3 mo after randomization (acute slope); (4) mean decline in GFR starting 3 mo after randomization (chronic slope); and (5) mean decline in GFR from baseline (total slope). The corresponding creatininebased outcomes were (1) a composite of doubling of serum creatinine, ESRD, or death and (2) a composite of doubling of serum creatinine or ESRD and acute, chronic, and total slopes defined by the mean change in estimated GFR (eGFR), where eGFR was estimated from a regression equation for GFR depending primarily on serum creatinine and developed in AASK enrollees. Mean changes in iGFR and eGFR were also compared under extended models that allowed for the possibility that the rate of GFR decline may change over time during the chronic phase. an apparent acceleration in rate of decline of renal function over time was found. Subtle differences were observed between effects of the interventions on some of the creatinine and iGFR slope-based outcomes, but the main conclusions of the trial were similar for the serum creatinine and iothalamatebased measurements. This has important implications for the design of clinical trials with renal outcomes.Choosing appropriate outcomes is critical to the success of clinical trials. In renal clinical trials to date, both slope-based and time-to-event renal outcomes have been used (1-5). In the slope-based analysis, GFR is estimated at multiple time points for all participants and curves constructed from these points that reflect the change in renal function over time. In most cases, constant slopes over time are assumed, and mean slopes are compared between the study groups to evaluate the effects of interventions on the rate of GFR decline. In time-to-event analysis, an event such as halving of GFR or ESRD is measured, and the time from randomization to the occurrence of these events is compared between the study groups.Inulin clearance is arguably the gold standard for accurately measuring GFR (6). In large clinical trials, however, 125

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Section: Discussionsupporting

confidence: 55%

A Comparison of Iothalamate-GFR and Serum Creatinine-Based Outcomes

Lewis¹,

Greene²,

Appel³

et al. 2004

Journal of the American Society of Nephrology

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“…In the series of Rutherford and colleagues (1977), rates varied as follows : glomerulonephritis 0.007-0.026, diabetes 0.003-0.038, polycystic kidneys 0.0015-0 .063, and pyelonephritis 0.000-0.014. The study (Rutherford et al 1977) also showed great variation from time to time in individual patients, with variations of over 10-fold.…”

Section: Nature Of the Underlying Diseasementioning

confidence: 99%

“…Many of these limitations are reduced when using serial observations in a given patient, but on occasions can have a profound influence on the relationships between plasma creatinine, creatinine clearance and renal function, vitiating attempts to plot or predict a steady course. Rutherford et al (1977) studied the course in 63 patients with diverse causes of renal failure. Although most patients seemed to pursue a steady course, with a single straight line relationship between 1/Cr and time, almost 20% of patients did not, and required the construction of 2 or more lines, implying an alteration in the slope at some point in their course.…”

Section: Mathematical Models Of Progression Of Renal Failurementioning

confidence: 99%

Preservation of Renal Function in Chronic Renal Failure.

Whitworth

Ihle²,

Becker³

et al. 1992

Tohoku J. Exp. Med.

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“…The attempt to repair damage begins with the recruitment of inflammatory cells but ends with an unchecked inflammatory response that activates matrixproducing cells leading to tubular cell apoptosis, irreversible scarring, loss of renal function, and ultimately ESRD [57] . The extent of damage rather than the underlying disease determines the outcome [58] . Progressive fibrosis is likely responsible for the disruption of glomerular and tubular architecture.…”

Section: Pathogenesismentioning

confidence: 99%

Stop chronic kidney disease progression: Time is approaching

Din¹,

Salem²,

Abdulazim³

2016

WJN

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Progression of chronic kidney disease (CKD) is inevitable. However, the last decade has witnessed tremendous achievements in this field. Today we are optimistic; the dream of withholding this progression is about to be realistic. The recent discoveries in the field of CKD management involved most of the individual diseases leading the patients to end-stage renal disease. Most of these advances involved patients suffering diabetic kidney disease, chronic glomerulonephritis, polycystic kidney disease, renal amyloidosis and chronic tubulointerstitial disease. The chronic systemic inflammatory status and increased oxidative stress were also investigated. This inflammatory status influences the antisenescence Klotho gene expression. The role of Klotho in CKD progression together with its therapeutic value are explored. The role of gut as a major source of inflammation, the pathogenesis of intestinal mucosal barrier damage, the role of intestinal alkaline phosphatase and the dietary and therapeutic implications add a novel therapeutic tool to delay CKD progression.

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Chronic progressive renal disease: Rate of change of serum creatinine concentration

Cited by 217 publications

References 18 publications

A Comparison of Iothalamate-GFR and Serum Creatinine-Based Outcomes

A Comparison of Iothalamate-GFR and Serum Creatinine-Based Outcomes

Preservation of Renal Function in Chronic Renal Failure.

Stop chronic kidney disease progression: Time is approaching

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