How fast does kidney function decline

Tubular toxicity of proteinuria. Nephrotoxicity and Chinese herbal medicine. Lim, CTS, R. Diabetes and glucose tolerance as risk factors for cardiovascular disease: the Framingham study.

Diabetes Care. Uk prospective diabetes studygroup. Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes UKPDS Br Med J. American Diabetes Association. Standards of medical Care in Diabetes abridged for primary care providers.

Clin Diabetes. Diabetic kidney disease. Nat Rev Dis Primers. Patients with type 2 diabetes having higher glomerular filtration rate showed rapid renal function decline followed by impaired glomerular filtration rate: Japan diabetes complications study. J Diabetes Complicat.

Fast renal decline to end-stage renal disease: an unrecognized feature of nephropathy in diabetes. Biomarkers of rapid chronic kidney disease progression in type 2 diabetes. Download references. Christopher Thiam Seong Lim, N. Fadhlina, M.

Anim, T. Kalaiselvam, W. You can also search for this author in PubMed Google Scholar. All of the authors are actively involved in the clinical care of the patients.

All authors read and approved the final manuscript. Correspondence to Christopher Thiam Seong Lim. Written informed consent was obtained from all three patients for publication of this Case Report and any accompanying images. Copies of the written consent is available for review by the Editor of this journal.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Reprints and Permissions. Lim, C. Rapid decline of renal function in patients with type 2 diabetes with heavy proteinuria: a report of three cases.

BMC Nephrol 20, 22 Download citation. Received : 01 May Accepted : 04 January Published : 16 January Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Fadhlina 1 , 2 , M. Kalaiselvam 1 , 2 , W. Abstract Background Although there is a large volume of literature regarding the definition and epidemiology of.

This is known as the glomerular filtration rate, or GFR. With time, many men's kidneys start to slip, but function must decline quite a lot before you start to really feel the impact. You feel fine up to the point that kidney function is almost gone, which means you can lead a normal life with reduced kidney function.

On the other hand, lack of early warning from symptoms can deny you the chance to slow the slide. As part of standard blood tests, your doctor can check the creatinine level to assess kidney function.

Creatinine is released from muscle cells into the blood stream. Creatinine is one of the things that the kidneys filter from the blood. If the kidneys start to lose some function, blood creatinine level rises. The creatinine level is used to calculate an estimate of the GFR and provide an estimate of your kidney function.

Most people who have a minor reduction in kidney function can take steps to not keep the kidneys from getting worse.

If the function is somewhat low but stable, you may need to see your doctor only once per year. If the GFR is declining or it is already under 50, it's best to see a kidney doctor, if for no other reason than to become educated. High blood pressure can cause tiny cracks in the lining of arteries, which provide a breeding ground for fatty deposits that hamper blood flow. As the arteries that feed blood to the kidneys narrow, the body produces renin, a hormone that makes small arteries narrow further.

This worsens high blood pressure, causing even more kidney damage. Over time, restricted blood flow can damage or destroy the nephrons, the tiny filtering units inside your kidneys. Keep your blood pressure and blood sugar within norms. This will help slow the decline in kidney function. Lower your cholesterol. In contrast, among patients without diabetes, those aged 50—69 years old were less likely than those aged 70—79 years old to have fast CKD progression.

However, conflicting results exist about the relationship between smoking history and longer-term endpoints such as the need for renal replacement therapy [ 35 , 36 ]. Lower hemoglobin levels below There have been conflicting data about the association between different lipoproteins and the risks of ESRD or significant loss of kidney function in adults with CKD.

Despite evaluating a wide range of candidate predictors of fast progression of CKD, our model discrimination was moderate for models in patients with c statistic 0. Importantly, however, model calibration i. This allowed us to examine annual rate of eGFR decline and to identify the subgroup of patients who experienced fast CKD progression. All relevant diagnoses, procedures, test results and treatments were comprehensively captured through a state-of-the-art electronic medical record system that facilitated assessment of relevant patient characteristics which may predict fast CKD progression.

Our study also had some limitations. For each patient, we calculated an average annual rate of eGFR decline estimated using linear regression, but patients may experience non-linear patterns of change in kidney function not reflected using this approach.

Similarly, results may not be completely generalizable to other clinical practice settings or to uninsured patients who may experience a different intensity of treatment or follow-up.

Even though we examined a wide range of patient characteristics, we cannot rule out residual confounding affecting our model results.

We were unable to comprehensively identify exposure to nephrotoxic insults or episodes of acute kidney injury from available data. Systematic information on other selected biomarkers that have been associated with different measures of CKD progression were also not available e. These findings may help in identifying the subset of patients who may benefit from more frequent monitoring of eGFR to identify fast CKD progression or proteinuria and subsequent intervention to potentially retard further loss of kidney function and other potentially associated adverse clinical outcomes such as cardiovascular events.

About predictors of acute kidney injury after lung resection. Anesth Analg. Article PubMed Google Scholar. CKD prevalence varies across the European general population. J Am Soc Nephrol. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med. Lifetime risk of ESRD. A predictive model for progression of chronic kidney disease to kidney failure. Risk models to predict chronic kidney disease and its progression: a systematic review.

PLoS Med. Predicting the risk of dialysis and transplant among patients with CKD: a retrospective cohort study. Am J Kidney Dis. Multinational assessment of accuracy of equations for predicting risk of kidney failure: a meta-analysis. Accessed 22 Dec Google Scholar. Past decline versus current eGFR and subsequent mortality risk. GFR decline and subsequent risk of established kidney outcomes: a meta-analysis of 37 randomized controlled trials.

Decline in estimated glomerular filtration rate and subsequent risk of end-stage renal disease and mortality. Association between chronic kidney disease progression and cardiovascular disease: results from the CRIC study. Am J Nephrol. Comparison of risk estimates for selected diseases and causes of death.

Prev Med. A community-based study of explanatory factors for the excess risk for early renal function decline in blacks vs whites with diabetes: the atherosclerosis risk in communities study. Arch Intern Med. Sukmark T, Sukmark S. Predictors of faster progression in chronic kidney disease. J Med Assoc Thail. A clinical stratification tool for chronic kidney disease progression rate based on classification tree analysis.

Nephrol Dial Transplant. Clin J Am Soc Nephrol. Variables that met this definition of confounding were retained. In addition, we compared mortality risk among participants who had rapid decline by eGFR creat only, eGFR cys only, neither, or both using unadjusted and multivariate-adjusted proportional hazards models. In addition, because of concern about regression to the mean, we considered 2 separate models: one that did not adjust for baseline eGFR, and a second model that adjusted for mean eGFR.

We examined the association of rapid decline based on the association of eGFR cys and eGFR creat within subgroups based on age, sex, race, and coronary heart disease.

Finally, we evaluated these associations within the subgroup of participants who were at low risk, defined as the absence of diabetes, hypertension, or cardiovascular disease at baseline, and compared the association with those participants with 1 or more of these risk conditions.

The purpose of this subgroup analysis was to evaluate whether decline in kidney function is associated with mortality risk even in a relatively low-risk subgroup.

Analyses were performed using S-Plus release 6. The individuals with 2 or 3 measurements of cystatin C and creatinine levels were younger, more likely to be female, and had substantially fewer cardiovascular risk factors, better baseline kidney function, and less cardiovascular disease at baseline than those with 0 or 1 measurement of cystatin C level.

Mean SD baseline creatinine and cystatin C levels were 0. First occurrences of cardiovascular disease coronary heart disease, stroke, transient ischemic attack, or congestive heart failure between the baseline and year 7 testings were more common in the group with rapid decline in eGFR cys.

Similar relationships were seen between those with and without rapid decline in eGFR creat Table 1. The point estimates were similar and statistically significant within each subgroup in Figure 2.

When results were stratified by baseline CKD, rapid decline was associated with similar increases in risk for all-cause and cardiovascular mortality. There were no significant interactions between rapid kidney function decline by eGFR cys or eGFR creat and age dichotomized at the median , race, sex, or baseline kidney function with either mortality end point.

These HRs were not different compared with the subgroup with at least 1 of these comorbidities at baseline Figure 2.

The group of participants with rapid decline by both eGFR creat and eGFR cys had all-cause and cardiovascular mortality rates nearly twice those of the group that did not meet either criterion Table 3. These associations with elevated risk were observed regardless of the initial eGFR. Rapid decline by either eGFR creat or eGFR cys was associated with elevations in mortality risk, and these associations were similar across subgroups of age, sex, race, cardiovascular disease, and baseline risk status.

While CKD is a well-established risk factor for all-cause and cardiovascular mortality, loss of kidney function within a population with relatively well-preserved kidney function has not previously been associated with adverse outcomes. It is noteworthy that this was a select population with a known risk factor for progression, whereas the CHS population was substantially larger, more heterogeneous, and more generalizable to the general population of older adults.

There are several reasons why loss of kidney function may be associated with increased mortality risk. Ongoing decline in kidney function may play a causal role by exacerbating cardiovascular disease risk factors such as hypertension and dyslipidemia or by causing retention of inflammatory solutes leading to oxidative stress and vascular damage. In addition, worsening kidney function may lead to decreased appetite, loss of lean body mass, decreased physical function, and overall frailty.

Overall, eGFR cys detected more individuals with decline in kidney function in this cohort than did eGFR creat , possibly reflecting that cystatin C is more sensitive to small changes in eGFR. However, participants with only eGFR creat rapid decline also had elevated mortality risk, which implies that change in eGFR cys has imperfect sensitivity for detecting high-risk individuals.

Although the CHS comprises a community-based, representative sample of older adults in the US, the individuals included in this analysis were selected for having survived long enough to have at least 2 measures of kidney function. These participants were healthier and had better kidney function on average than the full CHS cohort, so their magnitude of decline in kidney function was likely less than would have been observed in the overall cohort.

Nevertheless, even in this healthier subgroup, there was substantial variability in kidney function loss over time, and rapid declines of kidney function were strongly associated with mortality risk. Our study has several limitations. We do not have direct measurements of GFR and therefore cannot assess whether the changes we observed in eGFR by either cystatin C or creatinine are truly reflective of changes in kidney function.

Albuminuria was not measured at baseline in CHS, so we cannot comment on the role of this marker of kidney disease in mediating or modifying the relationships we observed. While regression to the mean may have led to misclassification bias, we considered several different statistical adjustments for baseline kidney function to account for this and noted that our results were robust regardless of the method used.

Although cystatin C appears to be a very sensitive marker of kidney function, it may be affected by thyroid dysfunction, corticosteroid use, and body composition, and cystatin C measurements may not reflect actual GFR as accurately at the extremes of body mass. Despite adjustment in multivariate models for both hypertension and diabetes mellitus, we cannot exclude the possibility of residual confounding from lifetime exposure to these conditions.