The kidney is a complex and vital organ, regulating the electrolyte and fluid status of the human body. As hemodialysis (HD) and peritoneal dialysis (PD) are forms of renal replacement therapy and not an actual kidney, they do not possess the same physiologic regulation of both fluid and electrolytes. Precise regulation of fluid and electrolytes in the HD and PD population remains a constant challenge. In this review, fluid status of both HD and PD will be examined, as well as sodium, potassium, phosphorous, and calcium. Each electrolyte will be analyzed by its physiological significance, the complications that arise when a proper balance cannot be maintained, and methods to correct these imbalances. An overview of the fluid compartments and volume of distribution within the body will be discussed. Ultrafiltration, a modality used in both forms of renal replacement therapy, will be defined, along with its impact on fluid status. Fluid assessment will be addressed, along with proper maintenance of fluid homeostasis. By having an understanding of the pathophysiology behind the fluid and electrolyte abnormalities that occur in end-stage renal disease, one can direct proper management with medications, diet, and alterations in dialysis to provide patients with the most optimal form of renal replacement therapy available.
Background. Kidney half-life and inter-stage progression rates in native chronic kidney disease (CKD) and CKD-transplant (CKD-T) remain unknown. Methods. We examined stage-to-stage progression/ regression rates in patients with CKD (n ¼ 601) and CKD-T (n ¼ 431) between 1991 and 2001. Kidney function was estimated by Cockcroft-Gault and MDRD eGFR formulae. Kaplan-Meier analyses determined progression and regression half-lives, defined as the time required for 50% of kidneys to advance towards a higher or lower stage of CKD, respectively. Results. Most (67%) of the patients were in stage 3. Patients with native CKD were more likely to progress compared to CKD-T (inter-stage progression rates 12 vs 4 cases per 100 patient-years, P < 0.0001). Accordingly, estimated glomerular filtration rate (eGFR)-based progression half-lives were significantly shorter in CKD compared to CKD-T [6 vs 9.6 years, P < 0.0001, hazard ratio (HR) 3.1, 95% confidence interval (CI) ¼ 2.5-3.7]. Creatinine clearance (CCR)-based stage half-lives were 7.2 months shorter in each group (5.4 and 9 years in CKD and CKD-T, respectively). Despite slower progression rates in patients with transplant kidney disease, adjusted patient survival rates were significantly decreased in CKD-T compared to CKD. Only Scr and CCR-based formulae were significantly associated with patient and allograft outcomes in the CKD-T group. Moreover, death rates were not different in stage 3 compared to stage 2 CKD-T, suggesting that eGFR and the current staging classification have a limited value to predict patient death in this cohort. Conclusion. Kidney half-lives per stage of CKD may be a novel tool to examine disease progression.
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