Having too much or too little of these electrolytes can have negative impacts on the body. The kidneys regulate what electrolytes we need through a process called reabsorption.

Reabsorption works by pulling needed electrolytes from the nephron tubules back into our blood, along with water and other small sized particles. When we have too much of a particular mineral the kidneys release the excess minerals into the tubule, to be released as waste.

This process is called excretion. Examples of important minerals that can be found in food are:. Health Science Information Consortium of Toronto LibGuides Exploring the Role and Function of the Kidneys Regulating electrolytes Search this Guide Search. Exploring the Role and Function of the Kidneys.

Thus, over 90 percent of the CO 2 is converted into bicarbonate ions, HCO 3 — , through the following reactions:.

The bidirectional arrows indicate that the reactions can go in either direction, depending on the concentrations of the reactants and products. Carbon dioxide is produced in large amounts in tissues that have a high metabolic rate. Carbon dioxide is converted into bicarbonate in the cytoplasm of red blood cells through the action of an enzyme called carbonic anhydrase.

Bicarbonate is transported in the blood. Once in the lungs, the reactions reverse direction, and CO 2 is regenerated from bicarbonate to be exhaled as metabolic waste. About two pounds of calcium in your body are bound up in bone, which provides hardness to the bone and serves as a mineral reserve for calcium and its salts for the rest of the tissues.

Teeth also have a high concentration of calcium within them. A little more than one-half of blood calcium is bound to proteins, leaving the rest in its ionized form. In addition, calcium helps to stabilize cell membranes and is essential for the release of neurotransmitters from neurons and of hormones from endocrine glands.

Calcium is absorbed through the intestines under the influence of activated vitamin D. A deficiency of vitamin D leads to a decrease in absorbed calcium and, eventually, a depletion of calcium stores from the skeletal system, potentially leading to rickets in children and osteomalacia in adults, contributing to osteoporosis.

Hypocalcemia , or abnormally low calcium blood levels, is seen in hypoparathyroidism, which may follow the removal of the thyroid gland, because the four nodules of the parathyroid gland are embedded in it. Hypercalcemia , or abnormally high calcium blood levels, is seen in primary hyperparathyroidism.

Some malignancies may also result in hypercalcemia. Phosphate is found in phospholipids, such as those that make up the cell membrane, and in ATP, nucleotides, and buffers.

Hypophosphatemia , or abnormally low phosphate blood levels, occurs with heavy use of antacids, during alcohol withdrawal, and during malnourishment.

In the face of phosphate depletion, the kidneys usually conserve phosphate, but during starvation, this conservation is impaired greatly. Hyperphosphatemia , or abnormally increased levels of phosphates in the blood, occurs if there is decreased renal function or in cases of acute lymphocytic leukemia.

Additionally, because phosphate is a major constituent of the ICF, any significant destruction of cells can result in dumping of phosphate into the ECF. Sodium is reabsorbed from the renal filtrate, and potassium is excreted into the filtrate in the renal collecting tubule.

The control of this exchange is governed principally by two hormones—aldosterone and angiotensin II. Figure 1. Recall that aldosterone increases the excretion of potassium and the reabsorption of sodium in the distal tubule. Aldosterone is released if blood levels of potassium increase, if blood levels of sodium severely decrease, or if blood pressure decreases.

Its net effect is to conserve and increase water levels in the plasma by reducing the excretion of sodium, and thus water, from the kidneys. In a negative feedback loop, increased osmolality of the ECF which follows aldosterone-stimulated sodium absorption inhibits the release of the hormone.

Angiotensin II causes vasoconstriction and an increase in systemic blood pressure. Angiotensin II also signals an increase in the release of aldosterone from the adrenal cortex.

In the distal convoluted tubules and collecting ducts of the kidneys, aldosterone stimulates the synthesis and activation of the sodium-potassium pump. Sodium passes from the filtrate, into and through the cells of the tubules and ducts, into the ECF and then into capillaries.

Water follows the sodium due to osmosis. Thus, aldosterone causes an increase in blood sodium levels and blood volume. Figure 2. Angiotensin II stimulates the release of aldosterone from the adrenal cortex. Calcium and phosphate are both regulated through the actions of three hormones: parathyroid hormone PTH , dihydroxyvitamin D calcitriol , and calcitonin.

All three are released or synthesized in response to the blood levels of calcium. PTH is released from the parathyroid gland in response to a decrease in the concentration of blood calcium.

The hormone activates osteoclasts to break down bone matrix and release inorganic calcium-phosphate salts.

PTH also increases the gastrointestinal absorption of dietary calcium by converting vitamin D into dihydroxyvitamin D calcitriol , an active form of vitamin D that intestinal epithelial cells require to absorb calcium.

PTH raises blood calcium levels by inhibiting the loss of calcium through the kidneys. PTH also increases the loss of phosphate through the kidneys. Calcitonin is released from the thyroid gland in response to elevated blood levels of calcium.

The hormone increases the activity of osteoblasts, which remove calcium from the blood and incorporate calcium into the bony matrix. Electrolytes serve various purposes, such as helping to conduct electrical impulses along cell membranes in neurons and muscles, stabilizing enzyme structures, and releasing hormones from endocrine glands.

The ions in plasma also contribute to the osmotic balance that controls the movement of water between cells and their environment.

Imbalances of these ions can result in various problems in the body, and their concentrations are tightly regulated. Aldosterone and angiotensin II control the exchange of sodium and potassium between the renal filtrate and the renal collecting tubule. Calcium and phosphate are regulated by PTH, calcitrol, and calcitonin.

dihydroxyvitamin D: active form of vitamin D required by the intestinal epithelial cells for the absorption of calcium.

Skip to main content. Module Fluid, Electrolyte, and Acid-Base Balance. Search for:. Electrolyte Balance Learning Objectives By the end of this section, you will be able to: List the role of the six most important electrolytes in the body Name the disorders associated with abnormally high and low levels of the six electrolytes Identify the predominant extracellular anion Describe the role of aldosterone on the level of water in the body.

Practice Question Watch this video to see an explanation of the effect of seawater on humans. Show Answer Drinking seawater dehydrates the body as the body must pass sodium through the kidneys, and water follows.

Critical Thinking Questions Explain how the CO 2 generated by cells and exhaled in the lungs is carried as bicarbonate in the blood.

How can one have an imbalance in a substance, but not actually have elevated or deficient levels of that substance in the body?

Show Answers Very little of the carbon dioxide in the blood is carried dissolved in the plasma. It is transformed into carbonic acid and then into bicarbonate in order to mix in plasma for transportation to the lungs, where it reverts back to its gaseous form.

Without having an absolute excess or deficiency of a substance, one can have too much or too little of that substance in a given compartment. This may be due to the loss of water in the blood, leading to a hemoconcentration or dilution of the ion in tissues due to edema. Licenses and Attributions.

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Although equally dangerous, hypokalemia is less common in CKD patients, as impaired renal K excretion usually leads to hyperkalemia. CKD patients can, however, still develop hypokalemia due to gastrointestinal K loss from diarrhea or vomiting or renal K loss from non-K-sparing diuretics.

K deficiency augments the detrimental impact of Na excess seen in patients on a regular Western diet. Converging evidence indicates a pathogenic role of combined high body Na and low K in the development of hypertension and hypertension-associated cardiovascular complications [ 26 ].

Moreover, K is capable of exerting vascular protective effects independent of its antihypertensive effect [ 27 ].

Acutely, severe hypokalemia can cause paralysis, ileus, and cardiac arrhythmias. Management involves K repletion and close monitoring. Post-dialysis hypokalemia has been associated with life-threatening cardiac arrhythmias and sudden cardiac deaths. The susceptibility to hypokalemia-triggered cardiovascular events could be related to the underlying cardiovascular diseases, occurring in a majority of ESRD patients [ 28,30 ].

Dialysis, especially with low K dialysate, predictably causes a large transmembrane K shift, which is thought to be a major contributor to the occurrence cardiac events. Low dialysate K and larger volume removal have been associated with higher rates of atrial fibrillation and higher rate of premature ventricular beats [ 31 ].

Other contributory factors include a long 2-day inter-dialytic interval [ 34 ,][ 35 ], rapid and large amounts of fluid removal, low dialysate calcium and Mg [ 33,36 ].

The challenge lies in balancing the need to treat pre-dialysis hyperkalemia and avoid post-dialysis hypokalemia. With declining kidney function, the capacity of bicarbonate conservation and generation decreases, while the net endogenous acid production in CKD remains unchanged, leading to the genesis of acidosis [ 38 ].

Notably, each residual-functioning nephron, however, undergoes hypertrophy and compensatorily generates a large amount of NH 3 [ 40,41 ]. Excess acid also increases endothelin-1 and aldosterone production [ 43,44 ], accelerating CKD progression [ 38,45,46,47 ].

In addition to promoting CKD progression, metabolic acidosis is known to cause protein catabolism, muscle wasting, bone demineralization, insulin resistance, impaired thyroid hormone and growth hormone secretion, exacerbation of β2 microglobulin accumulation [ 49,50 ] and increased mortality [ 46,51 ].

Taken together, metabolic acidosis is associated with accelerated CKD progression and elevated all-cause mortality. The beneficial effects of correcting acidosis have been noted in multiple studies [ 42,53,54,55 ]. Phisitkul et al. Interestingly, Goraya et al.

The upper target of the serum bicarbonate for CKD patients has not been established. Different studies have used varying target serum bicarbonate levels. There are several ongoing randomized clinical trials evaluating the effect of NaHCO 3 on renal function, rate of CKD, mortality, bone turnover markers, muscle strength and quality of life [ 60,61,62 ].

The results from these trials will clarify the effects of oral bicarbonate as well as an appropriate upper serum bicarbonate target. Most clinical data associated with acidosis are generated from CKD patients and not specifically from dialysis patients.

Given the known pathobiology of acidosis, we expect a similar negative impact on morbidity and mortality in dialysis patients.

A unique aspect of patients on hemodialysis is the exposure to a large fluctuation of the acid-base status with each dialysis episode, from varying degrees of pre-dialysis acidosis to alkalosis rapidly corrected by the dialysis.

The large pH swing in a short period of h could lead to a multitude of adverse effects. Moreover, bicarbonate binding of endogenous acid can cause rapid CO 2 accumulation and paradoxical intracellular acidosis, resulting in multiple cellular function defects. Taken together, the pre-dialysis acidosis and rapid correction of acidosis to the range of alkalosis by dialysis can negatively impact patient outcome.

Bicarbonate profiling during hemodialysis or graded bicarbonate dialysate might minimize the large acid-base swing. Further studies are needed to explore these potential strategies. Bone mineral metabolism and calcium-phosphorus homeostasis involve a complex interplay among kidneys, gut, bone and parathyroid glands.

The metabolism involves parathyroid hormone PTH , vitamin D and vitamin D receptors, fibroblast growth factor FGF23 , Klotho and calcium-sensing receptors. As regulated excretion of calcium and phosphate is carried out primarily by the kidney, kidney failure inevitably causes abnormalities in bone turnover and, in most cases, soft tissue and vascular calcification, leading to increased mortality.

This triad of laboratory abnormalities, bone disorder and soft tissue calcification is collectively termed MBD [ 64 ]. As CKD progresses, renal phosphate excretory capacity becomes exhausted, and hyperphosphatemia ensues [ 65,66,67 ].

Hyperphosphatemia, through PTH, causes an increased bone turnover and contributes to the development of osteitis fibrosa cystica and osteomalacia.

More importantly, hyperphosphatemia promotes osteo-chondrogenic transformation and apoptosis of vascular smooth muscle cells and vessel wall collagen matrix accumulation and mineralization [ 68,69,70 ].

Large cohort studies have consistently shown that hyperphosphatemia is associated with vascular calcification [ 71 ], CKD progression [ 72 ] and increased risk of cardiovascular events and mortality [ 73,74,75 ].

Collectively, the association of serum phosphorus with cardiovascular events and mortality begins at a high normal range of phosphorus [ 77,78,79 ] and occurs in patients at all stages of CKD [ 80,81 ], as well as in critically ill patients with dialysis-requiring acute kidney injury [ 75 ].

Causal relationship between hyperphosphatemia and CKD progression and mortality, however, remains to be established. Secondary hyperparathyroidism develops in CKD and ESRD patients due to hyperphosphatemia, hypocalcemia, 1,25 OH 2 vitamin D deficiency, skeletal resistance to vitamin D, and reduced expression of calcium sensing receptors [ 82 ].

In addition to decreasing proximal tubular phosphorus reabsorption and increasing distal calcium reabsorption, PTH increases the renal expression of 1α-hydroxylase and suppresses inactivating enzyme 24α-hydroxylase, leading to a net increase in the formation of 1,25 OH 2 vitamin D [ 83,84,85 ].

PTH increases bone turnover via the activation of both osteoclast and osteoblasts, and the effects are mediated through RANK ligand and the decoy protein osteoprotegerin [ 82 ]. Bone disorder in CKD-MBD varies widely from a high bone turnover state osteitis fibrosa cystica due to excessive PTH elevation to a low turnover, adynamic state, due often to PTH over-suppression.

The combined elevations of PTH, calcium and phosphorus in a uremic milieu create a pre-condition for the development of a highly fatal calcific uremic arteriolopathy calciphylaxis [ 86 ].

In addition, vitamin D has multiple pleiotropic effects including regulating cell growth, differentiation and immunity, anti-inflammatory response, neuron health, insulin secretion and lipid metabolism [ 87,88 ]. Vitamin D deficiency in patients with and without CKD is associated with increased mortality [ 89,90 ].

Vitamin D deficiency has also been associated with cardiovascular disease, decreased muscle strength, and decreased cognitive function. CKD patients are more prone to develop vitamin D deficiency [ 91 ].

FGF23, secreted by osteocytes in response to hyperphosphatemia, is a key phosphaturic and a vitamin D counter-regulatory hormone. It binds to FGF receptor-Klotho complex and decreases proximal tubular phosphate reabsorption by down-regulating Na-phosphate co-transporters Na-Pi 2a and 2c [ 93 ].

FGF23 also inhibits renal 1α-hydroxylase, and stimulates inactivating enzyme 24α-hydroxylase resulting in decreased 1,25 OH 2 vitamin D and 25 OH vitamin D respectively [ 94 ].

In the parathyroid gland, FGF23 binds to the FGF receptor-Klotho complex and inhibits PTH expression and secretion [ 95 ]. These effects, however, dissipate in CKD and ESRD due to a decreased expression of FGF receptor-Klotho complex [ 96 ].

FGF23 elevation is one of the earliest markers of BMD in CKD, much before the elevations PTH and phosphate [ 97 ] and an independent risk factor for left ventricular hypertrophy [ 98,99 ], cardiovascular events, CKD progression [ ] and mortality [ ].

The management of CKD-MBD is complex and consists of efforts to maintain serum phosphate and calcium levels within or near the normal range, supplement vitamin D or active vitamin D when appropriate, and treat secondary hyperparathyroidism.

Multiple studies have shown benefits of using non-calcium-based phosphate binders sevelamer, lanthanum, ferric citrate and sucroferric oxyhydroxide over calcium-based binders calcium acetate, calcium carbonate and calcium citrate in terms of lower mortality [ ,, ]. Other phosphate binders that have been explored are a combination of calcium acetate and magnesium carbonate CaMg.

CALMAG randomized controlled trial using CaMg versus sevelamer-HCl in a population of dialysis patients has demonstrated the effectiveness of CaMg complex in lowering serum phosphorus [ ]. In rodent CKD models, CaMg reduced arterial calcification, comparable to the effects of sevelamer-HCL, without over-suppression of bone turnover or skeletal Mg accumulation [ ,, ].

CaMg could potentially be an effective alternative to treat hyperphosphatemia. Further studies, however, are necessary. KDIGO CKD-MBD guidelines recommend avoiding an absolute PTH value-based target for non-dialysis CKD patients but to monitor the PTH trend and initiate therapy in the setting of prominent PTH rise.

For dialysis patients, a target PTH range of times the upper limit of normal is recommended [ ]. Cholecalciferol and ergocalciferol can be used to treat suboptimal vitamin D status; they may not suppress PTH secretion [ ]. Cinacalcet, a calcimimetic agent, has been approved by the FDA to treat secondary hyperparathyroidism in dialysis patients.

A recent observational study has shown beneficial effects of cinacalcet in lowering PTH, calcium and phosphate in non-dialysis CKD patients [ ]. For patients with tertiary hyperparathyroidism autonomous PTH production , therapeutic options are limited to cinacalcet or subtotal parathyroidectomy [ ].

Dysnatremia and dysmagnesemia are the other 2 major electrolyte alterations seen in CKD and ESRD. Etiology, clinical features and management strategies for the 2 derangements are largely similar to those in the general population.

Below, we focus on the unique aspects relevant to CKD and ESRD patients. Dysnatremia usually indicates a condition where body water becomes excess or deficient. CKD patients follow a similar pattern of dysnatremia distribution.

During a median follow-up of 5. A recent meta-analysis of 15 studies has shown a mortality benefit with improving hyponatremia [ ]. In addition to the causes of hyponatremia seen in the general population, CKD patients are at additional risk of hyponatremia due to compromised capacity to dilute or concentrate urine.

Furthermore, polypharmacy and limited nutritional solute intake [ ] are common and can contribute to the Na derangements. In dialysis patients, hyponatremia is mostly dilutional, due to excess water or hypotonic fluid intake.

Dysnatremia in CKD and ESRD has mortality significance. A U-shaped association between serum Na and mortality was found in both non-dialysis CKD [ , ] and dialysis patients [ , ]. The management of dysnatremia in CKD patients is similar to that for the general patients and should start with identifying and, if possible, correcting the underlying cause.

For dialysis patients, extra sessions of dialysis may be considered. Rapid correction for chronic dysnatremia should be avoided. Although etiology and manifestations of dysmagnesemia have been studied mostly in the general population, both hypo- and hypermagnesemia are common in hospitalized patients with reduced eGFR [ ].

Sustained hypermagnesemia is seen mostly in patients with advanced CKD and ESRD. Mg-containing medications may contribute to or exacerbate hypermagnesemia in the setting of kidney dysfunction. In dialysis patients, serum Mg is often affected by dialysate Mg content.

Sakaguchi et al. Similar results are shown in patients on peritoneal dialysis [ ]. Taken together, dysmagnesemia exerts morbidity and mortality significance in CKD and ESRD patients; care should be taken to correct Mg derangements. A variety of electrolyte and acid-base derangements predictably occur with progressive loss of kidney function.

Most of the derangements are intricately linked to morbidity and mortality. Prominently, hyperkalemia is linked to acute cardiac death in CKD and ESRD patients. Newer and more effective agents, patiromer and ZS-9, have the potential to mitigate hyperkalemia and improve patient outcomes, especially in those who benefit from RAAS inhibition.

Likewise, acidosis in renal failure patients should be carefully followed and corrected. Newer randomized controlled trials will further clarify our management strategy. MBD in CKD and ESRD remains a morbid condition.

Existing data suggest that non-calcium-containing phosphorus binders are associated with better cardiovascular outcomes. Newer pathogenic signaling pathways continue to be uncovered, and novel treatment targets will likely emerge in the near future.

Na and Mg derangements are reviewed in brief, given the space limitation. Both conditions, however, can be life threatening and should be carefully diagnosed and treated. Taken together, electrolyte and acid-base alterations form a major part of the pathological disease processes in patients with renal failure.

FDA has approved its use for non-dialysis CKD patients. It is not yet approved by the FDA. It can be lifesaving if ACE inhibitors and ARBs are given continuously for most of the CKD and ESRD patients. For ESRD dialysis patients, serum PTH should be within times the upper limit of the normal value.

Adjusting the dialysate Mg content may, thus, be necessary when appropriate. Careful evaluation of the patient's medications, both over-the-counter and prescribed agents, is necessary. Sign In or Create an Account. Search Dropdown Menu. header search search input Search input auto suggest.

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Volume 43, Issue Potassium Derangements. Metabolic Acidosis. Derangements of Bone Mineral Metabolism. Other Electrolyte Derangements. Key Messages. Disclosure Statement. Article Navigation. Review Articles January 24 Electrolyte and Acid-Base Disorders in Chronic Kidney Disease and End-Stage Kidney Failure Subject Area: Nephrology.

Tsering Dhondup ; Tsering Dhondup. Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, College of Medicine, Rochester, MN, USA. This Site. Google Scholar. Qi Qian Qi Qian. qi mayo. Blood Purif 43 : — Article history Published Online:. Cite Icon Cite.

toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. The authors have no conflicts of interest to declare. United States Renal Data System: USRDS Annual Data Report: Epidemiology of Kidney Disease in the United States.

Bethesda, National Institutes of Health, aspx cited October 8, De Nicola L, Zoccali C: Chronic kidney disease prevalence in the general population: heterogeneity and concerns. Nephrol Dial Transplant ; Luo J, et al: Association between serum potassium and outcomes in patients with reduced kidney function.

Clin J Am Soc Nephrol ; Sarafidis PA, et al: Prevalence and factors associated with hyperkalemia in predialysis patients followed in a low-clearance clinic.

Einhorn LM, et al: The frequency of hyperkalemia and its significance in chronic kidney disease. Arch Intern Med ; Chang AR, et al: Antihypertensive medications and the prevalence of hyperkalemia in a large health system.

Hypertension ; Ingelfinger JR: A new era for the treatment of hyperkalemia? N Engl J Med ; Meng QH, Wagar EA: Pseudohyperkalemia: a new twist on an old phenomenon. Crit Rev Clin Lab Sci ; Parham WA, et al: Hyperkalemia revisited.

Tex Heart Inst J ; Khattak HK, et al: Recurrent life-threatening hyperkalemia without typical electrocardiographic changes. J Electrocardiol ; Barold SS, Herweg B: The effect of hyperkalaemia on cardiac rhythm devices.

Europace ; Epstein M, et al: Evaluation of the treatment gap between clinical guidelines and the utilization of renin-angiotensin-aldosterone system inhibitors. Am J Manag Care ;21 11 suppl :SS Evans BM, et al: Ion-exchange resins in the treatment of anuria.

Lancet ; Lepage L, et al: Randomized clinical trial of sodium polystyrene sulfonate for the treatment of mild hyperkalemia in CKD. Harel Z, et al: Gastrointestinal adverse events with sodium polystyrene sulfonate Kayexalate use: a systematic review. Am J Med ; Li L, et al: Mechanism of action and pharmacology of patiromer, a nonabsorbed cross-linked polymer that lowers serum potassium concentration in patients with hyperkalemia.

J Cardiovasc Pharmacol Ther ; Weir MR, et al: Patiromer in patients with kidney disease and hyperkalemia receiving RAAS inhibitors. Bakris GL, et al: Effect of patiromer on serum potassium level in patients with hyperkalemia and diabetic kidney disease: the AMETHYST-DN randomized clinical trial.

JAMA ; Weir MR, et al: Treatment with patiromer decreases aldosterone in patients with chronic kidney disease and hyperkalemia on renin-angiotensin system inhibitors.

Kidney Int ; Gekle M, Grossmann C: Actions of aldosterone in the cardiovascular system: the good, the bad, and the ugly? Pflugers Arch ; Ritz E, Tomaschitz A: Aldosterone, a vasculotoxic agent - novel functions for an old hormone.

Bushinsky DA, et al: Effect of patiromer on urinary ion excretion in healthy adults. Clin J Am Soc Nephrol ;pii:CJN. Packham DK, et al: Sodium zirconium cyclosilicate in hyperkalemia.

Kosiborod M, et al: Effect of sodium zirconium cyclosilicate on potassium lowering for 28 days among outpatients with hyperkalemia: the HARMONIZE randomized clinical trial.

Bushinsky DA: National Kidney Foundation Spring Clinical Meetings Abstracts April May 1, Patiromer Decreases Serum Potassium in Patients on HD. Am J Kidney Dis ;A1-A Adrogué HJ, Madias NE: Sodium and potassium in the pathogenesis of hypertension. Tobian L, et al: Potassium reduces cerebral hemorrhage and death rate in hypertensive rats, even when blood pressure is not lowered.

Hypertension ;7 3 pt 2 :II Chiu DY, et al: Sudden cardiac death in haemodialysis patients: preventative options. Nephrology Carlton ; Collins AJ, et al: US Renal Data System Annual Data Report. Am J Kidney Dis ;63 1 suppl :A7.

Ohtake T, et al: High prevalence of occult coronary artery stenosis in patients with chronic kidney disease at the initiation of renal replacement therapy: an angiographic examination. J Am Soc Nephrol ; Buiten MS, et al: The dialysis procedure as a trigger for atrial fibrillation: new insights in the development of atrial fibrillation in dialysis patients.

Heart ; Pun PH, et al: Modifiable risk factors associated with sudden cardiac arrest within hemodialysis clinics. Jadoul M, et al: Modifiable practices associated with sudden death among hemodialysis patients in the Dialysis Outcomes and Practice Patterns Study.

Foley RN, et al: Long interdialytic interval and mortality among patients receiving hemodialysis. Bleyer AJ, et al: Characteristics of sudden death in hemodialysis patients.

Bleyer AJ, Russell GB, Satko SG: Sudden and cardiac death rates in hemodialysis patients. Santoro A, et al: Patients with complex arrhythmias during and after haemodialysis suffer from different regimens of potassium removal.

Vallet M, et al: Urinary ammonia and long-term outcomes in chronic kidney disease. Wrong O, Davies HE: The excretion of acid in renal disease. Q J Med ; The General Nephrology Clinic is located in the Taubman Center, reception area 3C.

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