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].

Hyperphosphatemia in dialysis: which binder?

Abstract

Several studies have evidenced the association between high serum phosphorus concentrations and adverse events especially in patients on dialysis.

Recent K-DIGO guidelines suggest lowering elevated phosphate levels toward the normal range. This goal should be achieved by combining dietary counseling, optimizing dialysis procedures and prescribing phosphate binders.

Despite the availability of several binders, the “ideal” phosphate binder that combines high efficacy, low pills burden, minimal side effects and low cost is still not available.
In clinical practice it is crucial to reach a high patient’s compliance to therapy. The pill burden is the most relevant factor contributing to low compliance. This is the case of phosphate binder therapy that represents almost 50% of total pills prescribed to patients on dialysis.
It has been evidenced an association between pills of phosphate binder and poor control of phosphorus and PTH.
In recent years sucroferric oxyhydroxide is available as a new phosphate binder. Its
peculiarity is an high phosphate binding capability that requires prescription of low number of pills per day. This characteristic has been confirmed by several randomized controlled trials. These trials have also evidenced that sucroferric oxyhydroxide may cause some gastrointestinal side effects. There is an ongoing study to confirm in “the real world” the incidence of side effects reported by controlled trials.

Key words: Phosphate; Binder; Secondary Hyperparathyroidism

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Lo scenario attuale

Le alterazioni del metabolismo minerale, ed in particolare l’iperfosforemia, sono riconosciute oggi fattori di rischio importanti per l’incremento della morbilità e mortalità dei pazienti affetti da malattia renale cronica, sia durante le fasi iniziali che nelle fasi più avanzate di malattia (1, 2).  Il controllo del bilancio fosforico rappresenta pertanto un punto cardine nel trattamento di questi pazienti.