Timing of the CKD Complications: A Longitudinal Analysis

Abstract

Background. Complications of chronic kidney disease include endocrine and metabolic abnormalities, anaemia and a wide range of disorders of homeostasis. Our study aims to better determine the role of CKD stage on the timing of the various complications associated with renal dysfunction.
Methods. We performed an observational study on 71 (F:M = 39:32) patients with 486 repeated measurements, recording anemia, BUN, hyperparathyroidism, hyperphosphatemia, hyperkalemia, metabolic acidosis. Data were summarized as mean and standard deviation, median and interquartile range, or absolute number. Differences among groups were tested through the Mann-Whitney test or Pearson’s Chi-Square. The associations between eGFR and each outcome was tested by Spearman’s correlation test. All variables related to the outcomes (with p-value <0.1) were included in the multivariate models. Longitudinal analysis was performed using generalized estimated equations (GEE) for binary outcome and by Linear Mixed Models for continuous variables. The ROC Curve with the Youden J index was evaluated for all binary outcomes. Results. Baseline analysis revealed hyperparathyroidism in 49 patients (69.1%), hyperphosphatemia in 11 patients (15.5%), hyperkalemia in 20 patients (28.6%), and mean serum urea was 78 mg/dl [IQR: 59-99]. CKD stage was related with all outcomes. Youden J index suggested an eGFR predictive value of 37 ml/min/m2 for anemia, 34 ml/min/m2 for hyperkalemia, 26 ml/min/m2 for hyperphosphatemia, and 46 ml/min/m2 for hyperparathyroidism.
Conclusion. Based on our findings, screening tests for endocrine and metabolic complications of CKD should be initiated at the beginning of the CKD stage III. We suggest screening for hyperphosphataemia at the CKD stage IV.

Keywords: Acidosis, Anemia, CKD, Parathormone, Phosphate, Potassium

Introduction

Chronic kidney disease (CKD) is characterized by an alteration of adequate metabolic homeostasis, increasing the risk of acidosis, hyperkalemia, hyperuricemia, hyperparathyroidism, hyperphosphatemia, and anemia.

This condition leads to a reduced excretory function, resulting in the accumulation of toxins in the body [1]. Among these catabolism products, urea is not completely excreted by the kidney when renal function is impaired.

As well for urea, renal filtration of hydrogen cations is altered when the residual nephron mass is impaired, increasing the risk of acidosis. Indeed, the severiry of acidosis is higher in patients with severe CKD [2]. Potassium removal is also reduced due to impaired renal function. Moreover, potassium is reabsorbed by proximal tubular cells through the exchange between H+ and K+ to correct acidosis [3].

Correction of secondary hyperparathyroidism with paricalcitol in renal transplant improves left ventricular hypertrophy

Abstract

Background – Left ventricular hypertrophy (LVH) is common in renal transplant recipients (RTRs), and persistent secondary hyperparathyroidism (SHPT) is considered to be one of the main causes of its pathogenesis. In this study we evaluated if the control of SHPT with paricalcitol is associated with a reduction of LVH in RTRs. Methods – For this purpose we selected 24 RTRs with LVH and SHPT . Secondary hyperparathyroidism was defined as PTH levels 1.5 times higher than the high normal limits, while LVH was defined as a left ventricular mass index (LVMi) >95g/m2 in females, and >115g/m2 in males. Treatment with paricalcitol started at mean dose of 1µg/day and lasted 18 months. The dose of paricalcitol was reduced to 1µg on the other day when serum calcium was >10.5mg/dl and/or fractional excretion of calcium was >0.020%; administration was temporarily stopped when serum calcium was >11 mg/dl. Results – At follow-up PTH levels decreased from 198 ± 155 to 105 ± 43pg/ml (P < .01), and LVMi decreased from 134 ± 21 to 113 ± 29g/m2 (P < .01); the presence of LVH decreased from 100% at baseline to 54% at F-U. Serum calcium levels showed a modest and not significant increase. Renal function was stable in all patients. Conclusions – Secondary hyperparathyroidism seems to play an important role in the development and maintenance of LVH and its correction with paricalcitol has a favorable impact on its progression.

Keywords: left ventricular hypertrophy; parathormone; paricalcitol; renal transplantation; secondary hyperparathyroidism

Sorry, this entry is only available in Italian.

INTRODUZIONE

La patologia cardiovascolare rimane una delle principali cause di morbilità e mortalità nel paziente portatore di trapianto renale (1). L’ipertrofia ventricolare sinistra (IVS) è uno dei principali reperti ecocardiografici nel trapianto renale riscontrandosi in circa il 50-70% di questi pazienti (2). L’evoluzione della IVS dopo trapianto renale rimane controversa.