The incidence of chronic kidney disease (CKD) in patients with chronic heart failure (CHF) is high as CKD and CHF share underlying risk factors such as arterial hypertension, diabetes mellitus and atherosclerosis. Cardiac failure leads to renal hypoperfusion and dysfunction and then fluid overload and need for aggressive diuretic therapy. However, development of diuretic resistance represents a significant problem in the management of these patients.
The role of Renal Replacement Therapy (RRT) is important for patients who do not response to conservative management of fluid overload facilitating the failing heart to restore function. According to the guidelines, venovenous isolated Ultrafiltration (UF) is indicated for patients with refractory congestion not responding to medical therapy with loop diuretics and infusion of dopamine. A systematic review of randomized controlled trials on the effect of UF vs. IV furosemide for decompensated heart failure showed a benefit of UF on total body weight loss and on readmissions due to heart failure in patients with decompensated heart failure and CKD. Peritoneal dialysis (PD) can provide efficient ultrafiltration and sodium extraction in volume overloaded patients followed by decline of hospitalization days, decrease of body weight and improvement of LVEF in patients with refractory heart failure. The continuous draw of ultrafiltrate is followed by a lesser risk of abrupt hypotension and better preservation of the residual kidney function. This represents a significant advantage of PD over intermittent UF by dialysis.
In conclusion, application of UF by dialysis and PD is followed by significant total body weight loss, reduced need for hospital readmissions and better quality of life. PD has a higher probability of preservation of residual kidney function and can be used by patients at home.
The traditional chronic kidney disease (CKD) biomarkers (eGFR based on serum creatinine, sex and age and albuminuria) cannot predict a patient’s individual risk for developing progressive CKD. For this reason, it is necessary to identify novel CKD biomarkers that will be able to predict which patients are prone to develop progressive disease and discriminate between disease processes in different parts of the nephron (glomeruli or tubules).
A good biomarker should change before or simultaneously with lesion development and its changes should correlate strongly with lesion development. Also, there should be a close relationship between severity of injury and amount of detectable biomarker and its levels should decrease with diminishing injury.
Among the large number of molecules under investigation, we have reviewed the most promising ones: NGAL and KIM-1, MCP-1, MMP-9, clusterin, MMP-9, TIMP-1, Procollagen I alpha 1 and suPAR. All these, have been studied as biomarkers for prediction of CKD progression in cohorts of patients with chronic kidney disease of different stages and various aetiologies (proteinuric and non-proteinuric, glomerulonephritides, diabetic, hypertensive and polycystic kidney disease). There is evidence that these molecules could be useful as biomarkers for progressive chronic kidney disease, however, the available data are not enough to draw final conclusions. Further studies with large cohorts and long follow-up are required to identify appropriate biomarkers, that will be able to accurately and reliably define the risk for progressive chronic kidney disease.
Introduction. Circulating autoantibodies against phospholipase A2 receptor (anti-PLA2R) are recognized as key elements in the pathogenesis of idiopathic membranous nephropathy. In current clinical practice, they are increasingly gaining attention as novel tools for diagnosis and disease monitoring. We investigated the diagnostic and prognostic utility of anti-PLA2R antibody measurements in Greek patients with biopsy-proven membranous nephropathy.
Methods. Anti-PLA2R levels were measured in serum samples from 33 patients at diagnosis using ELISA and were associated with treatment outcome. Moreover, serial anti-PLA2R measurements were performed in 15 patients under different clinical conditions and level alterations were correlated with disease activity.
Results. Positive anti-PLA2R antibodies at diagnosis were found in 16 of 33 patients (48.5%). Anti-PLA2R levels were independently associated with the achievement of complete remission of nephrotic syndrome after immunosuppressive treatment compared to partial remission (p = 0.02, R2 = 0.265, 95%CI -0.019 to -0.0003). Higher detectable antibody levels at diagnosis were correlated with higher proteinuria levels (r = 0.813, p = 0.0001, 95%CI 0.532 to 0.933) and lower eGFR at the end of follow-up (r = -0.634, p = 0.0083, 95%CI -0.86 to -0.202). Serial antibody measurements during follow-up showed that anti-PLA2R titers were significantly reduced at the end of treatment after complete remission was achieved, remained low under sustained clinical remission, and increased during relapse.
Conclusions. Our findings confirm the usefulness of anti-PLA2R measurements in the diagnosis of idiopathic membranous nephropathy. Low levels of anti-PLA2R antibodies at diagnosis are predictive of complete remission of nephrotic syndrome following immunosuppressive treatment. Serial anti-PLA2R measurements correlate well with clinical status throughout the follow-up period and could be used routinely for monitoring of disease activity and treatment planning.