Prevalence and progression of chronic kidney disease after renal transplantation

Background

We studied the prevalence of chronic kidney disease (CKD) and its progression after kidney transplantation.

Methods

We retrospectively analyzed the evolution of renal graft function, as estimated by the Cockcroft-Gault equation in 567 patients. CKD was classified in accordance with the National Kidney Foundation/Kidney Disease Outcome Quality Initiative with progression estimated by calculating the slope over time.

Results

Creatinine clearance (CrCL) at 1 year after transplantation was 57.8 ± 15.5 mL/min with 61.9% patients presenting de novo chronic renal failure. The 1-year-CrCl provided the best correlation with the 3-year CrCl (R² = 0.58; P < .001). Medians of slope (MS) among all patients was −2.38 ± 5.7 mL/min/y (−11.9 mL/min over 5 years). Patients who reached a CrCl < 60 at 1 year after transplantation showed a MS of −3.92 ± 6.5, while the others, −2.03 ± 5.2 mL/min/y (P = .046). Similarly, patients who reached a CrCL < 60 at 3 years after transplantation displayed a MS of −1.49 ± 3.5 mL/min/y, while the others, 0.62 ± 3.0 mL/min/y (P < .001).

Conclusions

The majority of renal transplant patients present de novo chronic renal failure already at 1 year posttransplantation. The rate of graft functional deterioration was 2.38 mL/min/y. It was worse among patients who displayed a CrCL less than 60 mL/min both at 1 and at 3 years. One-year CrCL was a good marker for 3-year CrCL.     

Disease severity and renal outcomes of patients with chronic kidney disease infected with COVID-19

Clinical and Experimental Nephrology - While there is evidence of the presence of the coronavirus in the kidneys and resultant acute kidney injury (AKI), information on the effect of chronic kidney...     

Inflammation in chronic kidney disease: role in the progression of renal and cardiovascular disease

Inflammation is the response of the vasculature or tissues to various stimuli. An acute and chronic pro-inflammatory state exists in patients with chronic kidney disease (CKD), contributing substantially to morbidity and mortality. There are many mediators of inflammation in adults with CKD and end-stage kidney disease (ESKD), including hypoalbuminemia/malnutrition, atherosclerosis, advanced oxidation protein products, the peroxisome proliferators-activated receptor, leptin, the thiobarbituric acid reactive system, asymmetric dimethyl arginine, iron, fetuin-A, and cytokines. Inflammation contributes to the progression of CKD by inducing the release of cytokines and the increased production and activity of adhesion molecules, which together contribute to T cell adhesion and migration into the interstitium, subsequently attracting pro-fibrotic factors. Inflammation in CKD also causes mortality from cardiovascular disease by contributing to the development of vascular calcifications and endothelial dysfunction. Similar to the situation in adults, cardiovascular disease in pediatric CKD is linked to inflammation: abnormal left ventricular wall geometry is positively associated with markers of inflammation. This review focuses on traditional and novel mediators of inflammation in CKD and ESKD, and the deleterious effect inflammation has on the progression of renal and cardiovascular disease.     

Metabolic syndrome in children with chronic kidney disease and after renal transplantation

Visceral obesity and metabolic abnormalities typical for metabolic syndrome (MS) are the new epidemic in adolescence. MS is not only the risk factor for cardiovascular disease but also for chronic kidney disease (CKD). Thus, there are some reasons to recognize MS as a new challenge for pediatric nephrologists. First, hypertensive and diabetic nephropathy, the main causes of CKD in adults, both share the same pathophysiological abnormalities associated with visceral obesity and insulin resistance and have their origins in childhood. Secondly, as the obesity epidemic also affects children with CKD, MS emerges as the risk factor for progression of CKD. Thirdly, metabolic abnormalities typical for MS may pose additional risk for cardiovascular morbidity and mortality in children with CKD. Finally, although the renal transplantation reverses uremic abnormalities it is associated with an exposure to new metabolic risk factors typical for MS and MS has been found to be the risk factor for graft loss and cardiovascular morbidity after renal transplantation. MS is the result of imbalance between dietary energy intake and expenditure inducing disproportionate fat accumulation. Thus, the best prevention and treatment of MS is physical activity and maintenance of proper relationship between lean and fat mass.     

The association of echocardiographic parameters on renal outcomes in chronic kidney disease

BackgroundPatients with chronic kidney disease (CKD) often have structural abnormalities of the heart due to pressure and volume overload. The aim of this study was to evaluate associations between echocardiographic parameters and renal outcomes (estimated glomerular filtration rate [eGFR] slope and progression to dialysis) in patients with stage 3–5 CKD.MethodsThis longitudinal study enrolled 419 patients. Changes in renal function were assessed using the eGFR slope. Rapid renal progression was defined as an eGFR slope < −3 mL/min/1.73 m²/year, and the renal endpoint was defined as commencing dialysis.ResultsIncreased left atrial diameter (LAD), ratio of left ventricular mass to body surface area (LVM/BSA), ratio of LVM to height^2.7 (LVM/ht^2.7), and ratio of observed to predicted LVM (o/p LVM) were associated with eGFR slope in an adjusted model, but left ventricular ejection fraction (LVEF) was not. Furthermore, LAD ≥ 4.7 cm, LVM/BSA > 115 g/m² in males and > 95 g/m² in females, and LVM/ht^2.7 > 48 g/ht^2.7 in males and > 44 g/ht^2.7 in females were correlated with progression to dialysis, but o/p LVM and LVEF were not. The maximum change in χ² change to predict renal outcomes was observed for LAD, followed by LVM/BSA and LVM/ht^2.7.ConclusionsA large LAD and increased LVM, regardless of how it was measured (LVM/BSA, LVM/ht^2.7 and o/p LVM), were correlated with adverse renal outcomes in patients with CKD stage 3–5. LAD had superior prognostic value to LVM and LVEF.     

Significant benefits after renal transplantation in patients with chronic heart failure and chronic kidney disease

Background: Chronic heart failure (CHF) and chronic kidney disease (CKD) are serious medical conditions with significant morbidity and mortality and often coexist. Because of perioperative risks in these patients, they may not be considered a candidate for renal transplantation (RTx).

Material and methods: We compare retrospectively RTx outcomes [graft/patient survival, rejection rates and adverse cardiac events] in study group [low left ventricular ejection fraction (LVEF) ≤45% by echocardiogram, n?=?63] and control group [normal LVEF ≥50%, n?=?537] from a developing country.

Results: The mean EF was 35?±?5.6 and 57?±?3% for the study and control groups, respectively (p?Conclusion: RTx may play a role in reversing LV systolic dysfunction. Once thought by many to be a contraindication for renal transplantation, this appears not to be the case. The outcomes between the 2 groups are comparable and transplant is an option for even low EF patients.     

Predicting initiation and progression of chronic kidney disease: Developing renal risk scores

Epidemiological studies have raised awareness of the problem of undiagnosed chronic kidney disease (CKD) and suggest that early identification and treatment will reduce the global burden of patients requiring dialysis. This has highlighted the twin problems of how to identify subjects for screening and target intervention to those with CKD most likely to progress to end-stage renal disease. Prospective studies have identified risk factors for CKD in the general population as well as risk factors for progression in patients with established CKD. Risk factors may thus be divided into initiating factors and perpetuating factors, with some overlap between the groups. In this paper, we review current data regarding CKD risk factors and illustrate how each may impact upon the mechanisms underlying CKD progression to accelerate loss of renal function. We propose that these risk factors should be used as a basis for developing a renal risk score, analogous to the Framingham risk score for ischemic heart disease, which will allow accurate determination of renal risk in the general population and among CKD patients.     

Cochlear function in chronic kidney disease and renal transplantation: a longitudinal study

Hearing loss on pure-tone and brainstem-evoked response audiometry is well documented in chronic kidney disease patients, but there are only scant data in renal allograft recipients. The aim of this study was to evaluate cochlear function on pure-tone and brainstem-evoked response audiometry among patients of chronic kidney disease to document changes after renal transplantation. The study included 20 healthy controls and 40 patients: 10 each at stage 3 and 4 and 20 with stage 5 chronic kidney disease. Patients with known causes for hearing loss were not included. Patients with stage 5 chronic kidney disease were reevaluated 1 year after renal transplantation. Compared with healthy controls, chronic kidney disease patients showed a highly significant bilateral sensorineural hearing loss at all frequencies of 0.25 to 8.0 kHz, which was more marked in higher frequencies. A highly significant delay in the latencies of waves I, III, and V and interpeak latencies of I to III and I to V was also noted on brainstem-evoked response audiometry. Compared with their pretransplant values, there was a significant improvement in the delay in absolute latencies of I, III, and V among renal allograft recipients. There was no correlation of audiometry findings with gender, degree of renal failure, and serum sodium. Hearing loss was seen in 70% of stage 3 and 4 chronic kidney disease and 60% in stage 5. The intensity of hearing loss was variable. In conclusion, chronic kidney disease patients shows definitive audiologic dysfunction with some improvement in hearing and wave latencies after successful renal transplantation.     

Disease management in chronic kidney disease

Chronic kidney disease (CKD) is a growing health problem of epidemic proportions both in the United States and worldwide. The care of CKD patients, before and after starting dialysis, remains highly fragmented resulting in suboptimal clinical outcomes and high costs, creating a high burden of disease on patients and the health care system. Disease management (DM) is an approach to coordinating care for this complex population of patients that has the promise of improving outcomes and constraining costs. For CKD patients not yet on dialysis, the major goals of a DM program are (1) early identification of CKD patients and therapy to slow the progression of CKD, (2) identification and management of the complications of CKD per se, (3) identification and management of the complications of comorbid conditions, and (4) smooth transition to renal replacement therapy. For those CKD patients on dialysis, focused attention on avoidable hospitalizations is a key to a successful DM program. Multidisciplinary collaboration among physicians (nephrologist, primary care physician, cardiologist, endocrinologist, vascular surgeons, and transplant physicians) and participating caregivers (nurse, pharmacist, social worker, and dietician) is critical as well. There are several potential barriers to the successful implementation of a CKD/end-stage renal disease DM program, including lack of awareness of the disease state among patients and health care providers, late identification and referrals to a nephrologist, complex fragmented care delivered by multiple providers in many different sites of care, and reimbursement that does not align incentives for all involved. Recent experience suggests that these barriers can be overcome, with DM becoming a promising approach for improving outcomes for this vulnerable population.     

Vitamin D and outcomes in chronic kidney disease

PURPOSE OF REVIEW: There is a high prevalence of vitamin D deficiency in the chronic kidney disease population. Vitamin D is often administered to patients to mitigate detrimental effects on bone health and mineral metabolism, though this treatment may be limited by elevations in serum calcium and phosphorus. This article reviews the basic physiology of vitamin D, the survival data in patients receiving vitamin D, and the current quandary of whether vitamin D administration is beneficial in chronic kidney disease. RECENT FINDINGS: Despite potential increases in serum calcium and phosphorus due to activation of vitamin D receptors in the gut, vitamin D administration has been associated with a survival benefit in recent studies. While the mechanism for this possible benefit is unknown, vitamin D administration may have effects beyond its traditional role in mineral metabolism, mediated through the activation of vitamin D receptors distributed in a variety of tissues. SUMMARY: Data currently suggests that the administration of vitamin D confers a survival benefit to patients on dialysis. There is no clear mechanism, however, to explain this association. Further research is needed to clarify the expanding role of vitamin D receptor activation, particularly in vascular calcification, and the effects of the different forms of vitamin D.     

Long-term outcomes in nondiabetic chronic kidney disease

The Modification of Diet in Renal Disease (MDRD) Study examined the effects of strict blood pressure control and dietary protein restriction on the progression of kidney disease. Here, we retrospectively evaluated outcomes of nondiabetic participants with stages 2-4 chronic kidney disease (CKD) from randomized and nonrandomized cohorts of the MDRD Study. Kidney failure and survival status through December of 2000, were obtained from the US Renal Data System and the National Death Index. Event rates were calculated for kidney failure, death, and a composite outcome of death and kidney failure. In the 1666 patients, rates for kidney failure were four times higher than that for death. Kidney failure was a more likely event than death in subgroups based on baseline glomerular filtration rate, proteinuria, kidney disease etiology, gender, and race. It was only among those older than 65 that the rate for death approximated that for kidney failure. In contrast to other populations with CKD, our study of relatively young subjects with nondiabetic disease has found that the majority of the participants advanced to kidney failure with a low competing risk of death. In such patients, the primary emphasis should be on delaying progression of kidney disease.     

Age affects outcomes in chronic kidney disease

Chronic kidney disease (CKD) is common among the elderly. However, little is known about how the clinical implications of CKD vary with age. We examined the age-specific incidence of death, treated end-stage renal disease (ESRD), and change in estimated glomerular filtration rate (eGFR) among 209,622 US veterans with CKD stages 3 to 5 followed for a mean of 3.2 years. Patients aged 75 years or older at baseline comprised 47% of the overall cohort and accounted for 28% of the 9227 cases of ESRD that occurred during follow-up. Among patients of all ages, rates of both death and ESRD were inversely related to eGFR at baseline. However, among those with comparable levels of eGFR, older patients had higher rates of death and lower rates of ESRD than younger patients. Consequently, the level of eGFR below which the risk of ESRD exceeded the risk of death varied by age, ranging from 45 ml/min per 1.73 m(2) for 18 to 44 year old patients to 15 ml/min per 1.73 m(2) for 65 to 84 year old patients. Among those 85 years or older, the risk of death always exceeded the risk of ESRD in this cohort. Among patients with eGFR levels <45 ml/min per 1.73 m(2) at baseline, older patients were less likely than their younger counterparts to experience an annual decline in eGFR of >3 ml/min per 1.73 m(2). In conclusion, age is a major effect modifier among patients with an eGFR of <60 ml/min per 1.73 m(2), challenging us to move beyond a uniform stage-based approach to managing CKD.     

Bariatric surgery and progression of chronic kidney disease

BackgroundObesity is an independent predictor for the development and progression of chronic kidney disease (CKD). The effect of weight reduction on the progression of kidney disease in patients with pre-existing CKD is unclear.MethodsWe conducted a retrospective study at a U.S. university hospital of patients with stage 3 CKD (glomerular filtration rate [GFR] 30–59 mL/min/1.73 m²) who had undergone bariatric surgery. The renal function of the included patients was recorded for a 2-year period after surgery to analyze the rate of loss or improvement in renal function. The estimated GFR was calculated using the Modification of Diet in Renal Disease 4-variable formula. Patients who developed acute renal failure in the postoperative period were excluded.ResultsA total of 25 patients with stage 3 CKD were included. Their average body mass index at surgery was 49.8 kg/m², the mean GFR was 47.9 mL/min/1.73 m², and the mean serum creatinine was 1.4 mg/dL. The body mass index had decreased to 38.4 kg/m² (paired t test, P < .001) at the end of 6 months and to 34.5 kg/m² (P < .001) at the end of 12 months. The mean systolic blood pressure had decreased from 133 ± 13 to 128 ± 17 mm Hg at the end of 12 months. The mean GFR at 6 months of follow-up had improved to 56.6 mL/min/1.73 m² (P < .001) and to 61.6 mL/min/1.73 m² (P < .001) at 12 months.ConclusionThe renal function of patients with CKD might improve after bariatric surgery. Larger and long-term studies are warranted to further analyze the effect of bariatric surgery on proteinuria and hard end-points such as the development of end-stage renal disease.     

Mechanisms of progression of chronic kidney disease

Chronic kidney disease (CKD) occurs in all age groups, including children. Regardless of the underlying cause, CKD is characterized by progressive scarring that ultimately affects all structures of the kidney. The relentless progression of CKD is postulated to result from a self-perpetuating vicious cycle of fibrosis activated after initial injury. We will review possible mechanisms of progressive renal damage, including systemic and glomerular hypertension, various cytokines and growth factors, with special emphasis on the renin–angiotensin–aldosterone system (RAAS), podocyte loss, dyslipidemia and proteinuria. We will also discuss possible specific mechanisms of tubulointerstitial fibrosis that are not dependent on glomerulosclerosis, and possible underlying predispositions for CKD, such as genetic factors and low nephron number.