Electrolyte and Acid-Base Disorders in Chronic Kidney Disease and End-Stage Kidney Failure

Abstract

The kidneys play a pivotal role in the regulation of electrolyte and acid-base balance. With progressive loss of kidney function, derangements in electrolytes and acid-base inevitably occur and contribute to poor patient outcomes. As chronic kidney disease (CKD) has become a worldwide epidemic, medical providers are increasingly confronted with such problems. Adequate diagnosis and treatment will minimize complications and can potentially be lifesaving. In this review, we discuss the current understanding of the disease process, clinical presentation, diagnosis and treatment strategies, integrating up-to-date knowledge in the field. Although electrolyte and acid-base derangements are significant causes of morbidity and mortality in CKD and end-stage renal disease patients, they can be effectively managed through a timely institution of combined preventive measures and pharmacological therapy. Exciting advances and several upcoming outcome trials will provide further information to guide treatment and improve patient outcomes.

Protein Nutrition and Malnutrition in CKD and ESRD

“…In dialysis patients requiring high protein intake, risk for hyperphosphatemia can be substantial and should be carefully monitored and when appropriate, phosphate binders should be promptly instituted [143]. A recent prospective study by Rhee et al of a cohort ( n = 110) of hypoalbuminemic hemodialysis patients showed beneficial effects of increasing serum albumin (≥0.2 mg/dL) and maintaining serum phosphorous levels within a target range (3.5 to <5.5 mg/dL) by providing high-protein meals during hemodialysis combined with lanthanum carbonate administration [144].…”

Toll-Like Receptor 9 Promotes Survival in SERCA2a KO Heart Failure Mice

“…We have previously shown that SERCA2a KO mice have a reduced LV inner diastolic diameter (LVID;d), subsequently necessitating a lower LV inner systolic diameter (LVID;s) to maintain stroke volume before acute decompensation [14]. This phenotype was seen in both HF groups, with no additional effect of TLR9 deficiency on LV dimensions (Figures 1(b) and 1(c)) nor on left atrium size (Figure 1(d)).…”

“…The sarcoplasmic/endoplasmic reticulum Ca 2+ ATPase (SERCA) is the main cytosolic Ca 2+ removal transporter and regulates cardiac relaxation [12]. We have previously shown that mice with cardiomyocyte-specific deletion of SERCA2a (SERCA2a KO) develop diastolic HF as compared with wild-type (WT) mice [13, 14]. Using this HF model, we demonstrated that chronic exposure to systemic TLR9 stimulations aggravated diastolic HF [14].…”

“…We have previously shown that mice with cardiomyocyte-specific deletion of SERCA2a (SERCA2a KO) develop diastolic HF as compared with wild-type (WT) mice [13, 14]. Using this HF model, we demonstrated that chronic exposure to systemic TLR9 stimulations aggravated diastolic HF [14]. However, systemic TLR9 stimulation caused severe systemic inflammation (including augmented cardiac inflammation) rendering it difficult to conclude whether the worsened cardiac function was a consequence of increased intrinsic cardiac TLR9 stimulation or was an indirect consequence of systemic inflammation.…”

Acid-Base and Electrolyte Managements in Chronic Kidney Disease and End-Stage Renal Disease: Case-Based Discussion

“…Patients with chronic kidney disease (CKD) and end-stage kidney failure (ESRD) are prone to develop metabolic derangements, especially acid-base and electrolyte imbalances [1]. Their presence imparts morbidity and mortality.…”