Etiologies

Hypokalemia may result from one of four possible etiologies: pseudohypokalemia; redistribution between cellular compartments; GI losses; and renal losses. In addition, hypomagnesemia is strongly associated with hypokalemia in malignancy, and contributes to kidney losses. Chemotherapy-induced decreased appetite and oral intake further confounds hypokalemia resulting from these losses. Typically, the etiology in cancer patients is largely “multifactorial,” and is summarized in Table 3.1 .

Workup and diagnosis of “true” hypokalemia are warranted after exclusion of pseudohypokalemia. The most common cause of pseudohypokalemia is acute leukemia, in which there are postphlebotomy transcellular shifts in the large number of abnormal leukocytes, if blood is stored in collection vials for prolonged periods, at room temperature. Rapid separation of plasma and storage at 4°C limits this issue.

Transcellular shifts of potassium in cancer patients are associated with malignancy-related medications and their adverse effects. Metabolic alkalosis from chemotherapy-induced vomiting, as well as alkaline volume expansion protocols, cause potassium to move intracellularly, as well as increased aldosterone activity resulting in increased potassium losses by the kidney. In addition, use of myelopoietic growth factors is associated with increased hematopoietic cell production, followed by rapid potassium uptake in the new cells. Similarly, increased production of blast cells in AML can also lead to hypokalemia.

GI losses in malignancy are largely caused by diarrhea that may occur because of chemotherapy, or radiation enteritis. Less commonly, villous adenoma or vasoactive intestinal secreting tumor (VIPoma) are associated with prolonged diarrhea and hypokalemia. ^, In addition, certain conditions in malignancy are associated with hypokalemia, secondary to upregulation of colonic/intestinal large-conductance calcium-activated potassium (BK) channels. ^, Hypokalemia associated with upper GI losses from vomiting or nasogastric suctioning is minimal, given the low (5–10 mEq/L) concentration of potassium in gastric secretions. The resulting hypokalemia is secondary to a combination of hypovolemia-induced aldosterone release, and increased bicarbonate delivery to the cortical collecting duct. The net effect is increased potassium secretion and urinary potassium wasting.

Potassium losses by the kidney in malignancy are associated with specific cancers and therapeutic agents and will be discussed in detail in the following sections. In addition, it is important to understand the mechanism of hypokalemia with concomitant hypomagnesemia, as it is frequently encountered in hypokalemia of malignancy. Luminal potassium secretion in the cortical collecting duct occurs via apical renal outer medullary potassium (ROMK) channels. Under physiologic conditions, intracellular magnesium binds ROMK and blocks potassium secretion. An increase in ROMK activity from magnesium deficiency (low intracellular magnesium) releases the magnesium-mediated inhibition of ROMK channels and increases potassium secretion. Additional factors for potassium secretion (distal sodium delivery, increased aldosterone levels) are essential for exacerbating potassium wasting and hypokalemia in magnesium deficiency ( Fig. 3.1 ). Hypomagnesemia in cancer patients may be caused by decreased intake or from increase urinary magnesium wasting. Losses of magnesium by the kidney are largely caused by chemotherapy-mediated injury to the distal nephron.

K ⁺ secretion by principal cells. The basolateral Na ⁺ K ⁺ ATPase lowers intracellular Na ⁺ concentration, and increases K ⁺ concentration. Entry of Na ⁺ via ENaC channels depolarizes the apical membrane, resulting in K ⁺ efflux via luminal ROMK channels. Flow-induced increases in K ⁺ secretion is mediated by BK channels. BK , Large-conductance calcium-activated potassium channels; ENaC , epithelial sodium channel; K ⁺ , potassium; Na ⁺ , sodium; ROMK , renal outer medullary potassium.

Hypokalemia associated with specific cancers

Among hematologic malignancies, hypokalemia is the most pronounced electrolyte abnormality in acute leukemia. Hypokalemia has been primarily described in patients with monocytic (M4) and acute myelomonocytic (M5) subtypes. It is mainly attributed to lysozymuria-induced renal tubular injury with kaliuresis. ^{, ,} Lysozyme is an enzyme originating from blood granulocytes and monocytes, as well as tissue macrophages. Lysozyme is normally reabsorbed in the proximal convoluted tubule. Lysozymuria occurring in patients with leukemia has been attributed to proliferation and destruction of lysozyme containing cells. Filtered lysozyme appears to be a direct tubular toxin. In addition, high levels of tubular lysozyme may induce significant kaliuresis and hypokalemia. Lysozymuria leading to profound hypokalemia has also been reported in chronic myelogenous leukemia. There have also been reports of renin-like activity in leukemic cells, stimulating the mineralocorticoid pathways and increasing potassium secretion by the kidney. ^,

Additional cancer-specific disorders associated with hypokalemia include disorders of mineralocorticoid excess. Although most adrenal adenomas are nonfunctional, up to 15% can be functional, secreting increased amounts of cortisol, which overwhelm 11-beta-hydroxysteroid dehydrogenase’s ability to metabolize cortisol to cortisone. Thus cortisol is able to bind the mineralocorticoid receptor and stimulate potassium excretion via ROMK channels ( Fig. 3.2 ). Adrenal carcinomas are rare and present with signs and symptoms of elevated cortisol levels. ^,

K ⁺ secretion with adrenal adenomas. Cortisol activates the mineralocorticoid receptor, resulting in increased ENaC, and subsequent ROMK activity. 11 β HSD converts cortisol to cortisone, which does not have mineralocorticoid activity. Increased amounts of cortisol exceed the ability of 11 β HSD to metabolize cortisol. Aldo , Aldosterone; ENaC , epithelial sodium channel; K ⁺ , potassium; MR , mineralocorticoid receptor; Na ⁺ , sodium; ROMK , renal outer medullary potassium; 11 β HSD , 11 beta hydroxyl steroid dehydrogenase.

Proximal tubular toxicity resulting from κ light chain myeloma, resulting in Fanconi syndrome is an indirect cause of malignancy associated hypokalemia. In dysproteinemias, the degree of filtered light chains exceeds the proximal tubule’s resorptive capacity, resulting in light chain proteinuria. Proximal tubule endocytosis of these light chains results in intracellular oxidative stress and cell apoptosis. The resulting proximal tubular disorder is Fanconi syndrome, with bicarbonaturia, glycosuria, aminoaciduria, phosphaturia, hyperuricosuria, and potassium wasting. Hypokalemia in proximal renal tubular acidosis results primarily in cases of supplemental bicarbonate repletion.

Other rare causes of cancer-specific hypokalemia include ectopic adrenocorticotropic hormone (ACTH) producing tumors. These include small-cell lung cancer, bronchial carcinoid tumors, lung adenocarcinomas, thymic tumors, pancreatic tumors and medullary thyroid cancer. Up to 30% of ectopic ACTH syndrome may present as occult tumors.

Hypokalemia association with therapeutic agents

Several drugs commonly used to treat cancer patients are contributory to development of hypokalemia. The mechanisms of common causative antimicrobials will be discussed briefly, before detailed discussions on chemotherapeutic agents.

Common antibiotics causing hypokalemia include aminoglycosides, amphotericin B, and penicillins. Aminoglycoside antibiotics are endocytosed in the proximal tubular cells, causing mitochondrial damage, and proximal tubule dysfunction. This results in a Fanconi-like syndrome, along with distal tubular dysfunction, resulting in hypomagnesemia, and subsequent hypokalemia. ^, The aminoglycosides may also cause a Bartter-like syndrome with sodium, potassium, and magnesium wasting. It is thought that these cationic drugs activate the calcium-sensing receptor in the loop of Henle tubular cells, which decreases Na ⁺ K ⁺ 2Cl ^– transport activity ( Fig. 3.3 ). Similarly, amphotericin B, commonly used in cancer patients for the treatment of fungal infections creates pores in cell membranes, resulting in increased membrane permeability. Increased permeability results in diffusion of potassium ions from distal tubule cells, and subsequent urinary potassium wasting. Lastly, penicillins have also been associated with hypokalemia, because of penicillin being a nonreabsorbable anion present in the distal tubule. The luminal electronegativity results in increased potassium excretion.

Aminoglycoside induced Bartter-like syndrome, with drug binding to CaSR, resulting in inhibition of NKCC activity, decreased ROMK channel back leak of potassium, with resulting decrease in paracellular Ca ²⁺ and Mg ²⁺ transport. Cl ⁻ , Chloride; CaSR , calcium sensing receptor; K ⁺ , potassium; Na ⁺ , sodium; ROMK , renal outer medullary potassium.

Cisplatin is a platinum-based chemotherapeutic agent, causing direct nephrotoxicity, with proximal tubular necrosis and distal tubule apoptosis. The mechanism of cisplatin-induced hypokalemia results mainly from proximal tubular injury and development of Fanconi syndrome, as well as marked hypomagnesemia ( Fig. 3.4 ). Tubular defects from cisplatin use can be permanent in certain cases. ^,

Cisplatin-induced hypokalemia. Cisplatin is taken up by organic ion transporters on the basolateral membrane. High concentrations of intracellular cisplatin lead to cell death and proximal tubular damage concentrated in the S3 segment, and development of a Fanconi-like syndrome. In the distal tubules, TRPM-6 magnesium channels are downregulated (possibly caused by loss of epithelial growth factor) leading to hypomagnesemia and obligate renal potassium wasting. DCT, Distal convoluted tubule; Mg ²⁺ , magnesium; PCT, proximal convoluted tubule; TRPM-6 , transient receptor potential subfamily melastatin.

Ifosfamide is an alkylating agent used in certain cancers. Nephrotoxicity secondary to ifosfamide includes proximal tubules (Fanconi syndrome), as well as distal tubules (nephrogenic diabetes insipidus, distal renal tubular acidosis). The metabolite chloracetaldehyde is directly toxic to cells, causing glutathione depletion and lipid peroxidation. ^, Adverse effects on kidney function can occur up to 10 years after ifosfamide administration. ^,

Epithelial growth factor receptor (EGFR) is a protein, which can be overexpressed by several different tumors: colorectal, lung, breast, pancreas, and head and neck cancers. It is important in modulating several cellular signaling pathways, making it a target for development of chemotherapeutic agents. EGFR monoclonal antibody inhibitors, such as cetuximab and panitumumab, have been shown to cause hypokalemia (up to 14.5% patients) secondary to hypomagnesemia (up to 34% patients). The mechanism of hypomagnesemia is thought to be related to magnesium permeable channels in the distal tubule, mainly transient receptor potential melastatin channel 6 and 7 (TRPM 6 and TRPM 7). EGF and TRPM 6 and 7 are both expressed in the distal convoluted tubule, and magnesium loss results from inhibition of EGF-mediated stimulation of TRPM activity ( Fig. 3.5 ). ^,

Absorption of magnesium is via EGFR-dependent apical channels, TRPM 6 and 7. This pathway is inhibited by anti-EGFR monoclonal antibodies (cetuximab and panitumumab). EGF , Epithelial growth factor; EGF-R , epithelial growth factor receptor; Mg ²⁺ , magnesium; TRPM6 , transient receptor potential melastatin 6.

Targeted melanoma therapy because of inhibition of the oncogenic BRAF V600 molecule, or a downstream signaling partner mitogen activating protein kinase (MAP kinase) has been shown to be effective in melanoma patients with BRAF mutations. Vemurafenib and dabrafenib (BRAF inhibitors) have been shown to be associated with hypokalemia. The mechanism is thought to be secondary to Fanconi syndrome.

Management

Once laboratory measurements confirm the presence of true hypokalemia, two urinary tests are commonly used to assess renal potassium losses. The fractional excretion of potassium (FE _K ) and the transtubular potassium gradient (TTKG) may provide insight into the kidney response to hypokalemia: FE _K would have an expected value of less than 2% in hypokalemia, and the TTKG would have an expected value of less than 2 in hypokalemia. More recently, the use of the TTKG has been called into question, and this should not be relied on solely to diagnose hypokalemia. Optimal correction of hypokalemia warrants a diagnosis of the cause and treatment of underlying disorder. Underlying acid-base disturbances should be investigated and corrected before potassium repletion.

Initial potassium replacement in cancer patients is the same as that in the general population. Given that approximately only 2% of total body potassium is in the extracellular fluid, along with high sensitivity to cellular shifts, serum potassium concentration is not a reliable marker of total body deficits. However, estimates indicate that a serum potassium concentration of less than 3 mmol/L or 2 mmol/L generally indicates deficits of around 200 mmol or 500 mmol respectively. Once the deficit is estimated, potassium supplementation can be administered orally or intravenously, usually as potassium chloride (KCl). Alternatively, potassium citrate can be used, particularly in patients with metabolic acidosis. Given potential GI side effects with oral KCl, cancer patients may possibly require intravenous KCl administration. Moreover, intravenous potassium repletion may be needed, given potential difficulty with oral intake caused by nausea, dysphagia, and mucositis. A rate of 20 mmol/h should not be exceeded, given the risk of rebound hyperkalemia. A recent study noted 16% of hospitalized patients developed hyperkalemia following correction of hypokalemia. The risk of hyperkalemia was associated with hematologic malignancies, as well as administration of total parenteral nutrition, both conditions commonly seen in cancer patients. Potassium sparing diuretics (amiloride, spironolactone, eplerenone, triamterene) can be used for chronic hypokalemia; however, there is an increased risk of hyperkalemia in patients with reduced kidney function, and concomitant administration of nephrotoxic medications. Potassium supplementation is ineffective if hypomagnesemia remains uncorrected, given ongoing potassium losses via ROMK channels. Intravenous magnesium repletion is usually needed because diarrhea is noted to be a dose limiting adverse effect of oral magnesium supplementation. Finally, long-term potassium repletion may be anticipated in some cases. As noted previously, anticancer agents, such as ifosfamide and cisplatin, may lead to persistent or even permanent potassium wasting.

Artefactual hyperkalemia

Spurious elevations of potassium in laboratory samples have been generally termed pseudohyperkalemia . This finding is most often associated with the elevated white blood cell (WBC) levels and platelets seen in various forms of leukemia and severe thrombocytosis. Potassium measurements may be made using serum, plasma, or whole blood samples. Traditionally, pseudohyperkalemia refers to elevated serum potassium concentration, with a significantly lower potassium concentration, when a plasma test is measured. Some authors define the presence of pseudohyperkalemia when the serum potassium is greater than 0.4 mmol/L above the plasma values. “Reverse” pseudohyperkalemia, a more recently described entity, refers to a falsely elevated plasma potassium and normal serum level. Numerous factors have been noted to contribute to artefactual potassium elevation including: venipuncture trauma leading to hemolysis, hand clenching, tourniquet technique, use of pneumatic transport tubes, type of specimen container used, and certain familial disorders leading to red cell fragility. The precise etiology of reverse pseudohyperkalemia is unclear but some have suggested the combination of fragile WBCs in disorders, such as chronic lymphocytic leukemia (CLL) and the use of heparinized collection tubes for plasma, which results in potassium leakage/membrane disruption during tube transport and centrifugation. Both types of artefactual potassium elevation have been associated with dialysis initiation and risk of subsequent hypokalemia. ^, A study of 57 CLL patients from Katkish and colleagues, in the Veterans Affairs system, described the probability of pseudohyperkalemia occurrence at 8.1% in those with WBC of 100.0 × 10 ⁹ /L or more over 270 patient years of follow-up. Assessing the presence of pseudohyperkalemia requires a high index of suspicion. Many case reports note a surprising lack of electrocardiogram changes despite significantly elevated potassium levels. ^, In a series of six patients with various leukemias, Dastych and Cemrakova found that the most reliable method for avoiding artefactual potassium rise was the use of a plasma sample in a heparinized tube (absent separator gel), walked manually to the laboratory. This resulted in a greater than 6.0 mmol/L difference in the potassium of one patient with acute lymphocytic leukemia: 3.9 mmol/L versus more than 10.0 mmol/L. Thus patients with hyperkalemia and hematologic malignancies require judicious interpretation of potassium values to avoid inadvertent initiation of potassium lowering therapies.

Cellular shifts/tumor lysis syndrome

Short-term (seconds to minutes) potassium management occurs primarily under the influence of insulin and catecholamines, resulting in cellular shifts of potassium, typically into and out of skeletal muscle. Elimination of potassium via renal and GI routes follows in the ensuing hours. In cases of normal renal function, the kidneys excrete around 90% of excess potassium intake and the GI tract excretion handles the remainder. In settings such as CKD or end-stage kidney disease (ESRD), a larger portion of potassium excretion can shift to the GI tract using BK channels, particularly of the colon, for enhanced excretion.

TLS (discussed in detail in Chapter 30 ) has the potential for rapid rise in plasma potassium levels. Potassium is the major intracellular monovalent cation, and total body stores may equal around 3500 mEq in a 70-kg individual with a distribution of 98% intracellular versus 2% extracellular. The classic description of TLS involves spontaneous or chemotherapy-induced malignant cell lysis with resultant release of high volumes of uric acid, potassium, and phosphorous. Once associated with mainly hematologic malignancies, TLS has been rarely described in solid tumors as well. The large volume of potassium release may overwhelm compensatory mechanisms, particularly in patients with acute disease or CKD. TLS occurring in the setting of preexisting CKD or following TLS-induced AKI may further exacerbate hyperkalemia. If prophylactic and temporizing measures fail, treatment of TLS-associated hyperkalemia may require renal replacement therapy. Given the ongoing release of potassium, prolonged dialysis may be necessary, such as continuous renal replacement therapy (CRRT) or slow low efficiency dialysis. If the initial potassium is markedly elevated, hemodialysis, with its more efficient potassium clearance, is the initial modality, which can then be followed by a period of CRRT—a management plan similar to that used in Lithium ingestion.

Cellular potassium shifts may also occur in the setting of acidosis or hyperglycemic states. Specific to cancer therapies, posttransplant diabetes mellitus (PTDM) may affect up to 30% of hematopoietic stem cell transplant survivors within 2-years posttransplant. This is thought to be mediated, in part, by injury of pancreatic β cells and increased insulin resistance mediated by calcineurin inhibitors, and the use of corticosteroids. Undiagnosed PTDM may present as diabetic ketoacidosis or hyperglycemic hyperosmolar states with accompanying hyperkalemia from osmolar shifts. Tacrolimus, in particular, has been more often associated with the onset of this condition versus cyclosporine in solid organ transplant recipients.

Finally, in addition to TLS, rhabdomyolysis has the potential to release large volumes of potassium from the intracellular stores. Various chemotherapy agents, given alone, in combination, or in combination with synergistic medications, such as statins, have been linked to rhabdomyolysis. For example, abiraterone, a treatment for castration resistant prostate cancer, has been reported to cause rhabdomyolysis, AKI, and hyperkalemia in association with statin use as has the vascular EGF tyrosine kinase inhibitor, pazopanib. ^{, ,} Other agents have also been implicated in cases of rhabdomyolysis and include myeloma therapies lenalidomide and bortezomib, the EGF-receptor inhibitor erlotinib, the tyrosine kinase inhibitors sunitinib and imatinib, and certain combination therapies.

Low aldosterone and low aldosterone-like states

Adrenal metastases are the most common adrenal lesions—far outnumbering primary adrenal cancers. This is attributed to generous sinusoidal blood supply of the adrenal glands. Despite the high prevalence of metastatic disease, clinical symptoms of adrenal insufficiency in these cases are rare. In a single center retrospective review of 464 patients with adrenal metastases over 30 years, only five patients presented with clinical signs/symptoms of adrenal insufficiency (Addison disease). This is attributed to the fact that a large volume of adrenal tissue must be destroyed (90%) before symptoms and laboratory abnormalities develop. Direct metastatic involvement has presented as adrenal insufficiency with hyperkalemia in several cancers including lung, breast, colorectal, and stomach among others. Surgical resection of metastatic disease in solid tumor cancers may also induce iatrogenic adrenal insufficiency and hyperkalemia.

In addition to solid tumors, leukemia has also been associated with idiopathic adrenal insufficiency and hyperkalemia. Li, recently reported the case of a 64-year-old man with undiagnosed AML, presenting with the classic electrolyte abnormalities of hyponatremia and hyperkalemia. A Turkish case series of 13 patients, with hyperkalemia and acute leukemia, demonstrated six with adrenal insufficiency of unclear etiology that resolved with disease remission. The authors suggest the presentation of hyperkalemia without an obvious attributable cause in acute leukemia, more often associated with hypokalemia, should prompt screening for adrenal insufficiency. Primary adrenal lymphoma, a rare presentation of extranodal lymphoma, may also produce adrenal insufficiency in more than 60% of patients with resulting hyperkalemia.

As one might expect, the treatment of primary adrenal lesions, such as aldosterone producing adenomas (APA), and the rarer adrenal adenocarcinoma, are often linked with adrenal insufficiency and hyperkalemia. A case series of patients undergoing adrenalectomy for APA reported almost 30% of patients developed hyperkalemia postoperatively. In adrenal adenocarcinoma, the use of mitotane in advanced stage disease has also been associated with adrenal insufficiency and electrolyte abnormalities (17% and 80%, respectively), and early replacement of glucocorticoids and fludrocortisone is recommended to avoid Addisonian crisis and hyperkalemia.

Direct medication effects

Although many anticancer agents may result in nephrotoxicities with the widely known complication of hypokalemia, relatively few agents are known to cause hyperkalemia in the absence of associate kidney failure. One example, the immunomodulatory drug thalidomide, gained popularity in the treatment of myeloma in the 1990s and early 2000s. It is still occasionally used in refractory or relapsed cases and has been associated with severe, sometimes fatal, hyperkalemia during the first few weeks of treatment in patients with CKD and ESRD. ^, The mechanism of hyperkalemia remains undetermined, but careful monitoring of patients with diminished GFR or on dialysis is warranted when using thalidomide. Hydroxyurea, a long-used medication for many hematologic diseases including polycythemia vera, sickle cell disease, and essential thrombocytosis (among others), has been linked to hyperkalemia in at least one case report. The patient in that case had rapid resolution of hyperkalemia with drug withdrawal and recurrence following reintroduction.

Calcineurin inhibitors (CNIs) prescribed following hematopoietic stem cell transplant (HSCT) have also been directly implicated in hyperkalemia. The mechanism now appears to be threefold. Originally it was thought that afferent arterial vasoconstriction leading to decreased GFR likely reduced clearance of potassium. Caliskan and colleagues, however, described a series of patients with hyperkalemia following allogeneic stem cell transplant despite normal renal function, suggesting an additional etiology. This second proposed mechanism is via disruption of the Na-K ⁺ adenosine triphosphatase (ATPase) on the basolateral membrane of the principal cell. This reduces the gradient for sodium transport through the luminal epithelial sodium channel and leads to decreased distal sodium-potassium exchange. The increased luminal sodium concentration also results in inhibition of proton secretion and resulting acidosis—reminiscent of a “type 4” renal tubular acidosis. Finally, in mouse models, tacrolimus has been shown to increase activation and trafficking of the sodium-chloride channel (NCC) in the distal convoluted tubule. Horn and colleagues determined that the increased NCC activity occurred because of increases in “with no lysine” kinases 3 and 4 as well as the STE20-related kinase. The net effect is increased sodium retention and, in mice fed a high potassium diet, hyperkalemia. The clinical picture is reminiscent of familial hyperkalemic hypertension. The trimethoprim component of trimethoprim-sulfamethoxazole, used for infection prophylaxis during the high dose steroid treatment of graft-versus-host disease, is another well-documented cause of hyperkalemia. As opposed to the indirect effect of CNIs, trimethoprim directly blocks the epithelial sodium channel in the distal nephron, reducing sodium-potassium exchange in an amiloride-like effect, with resulting hyperkalemia.

Treatment

Like all potassium abnormalities, diagnosis of the underlying cause of hyperkalemia in cancer patients is required for long-term management. In life-threatening scenarios, the usual methods of stabilization of the cardiac membrane, intracellular shifting of potassium, and promoting excretion via renal and GI mechanisms, remain guiding principles ( Fig. 3.6 ). Dialysis is used when necessary for the usual indications. However, there are special considerations in patients with cancer. For example, by definition, TLS is accompanied by hyperkalemia. Various risk prediction scores have been proposed to assess the likelihood of TLS for a particular patient and can allow anticipatory counseling for patients, prophylactic therapy, and early preparations by the oncology and nephrology care teams. ^, The usual prophylaxis of enhanced distal sodium delivery via intravenous crystalloid and volume delivery is usually enough to prevent life-threatening hyperkalemia. However, if AKI is encountered with oliguria and hyperkalemia, renal replacement therapy (RRT) may be indicated. There are no trials to support preemptive RRT in high risk patients; however, the clinician may expect a prolonged period of potassium release (potentially days) in cases of severe TLS. In these situations, intermittent hemodialysis to rapidly clear excess potassium may be indicated along with a period of continuous therapy. Alternately, if potassium has not reached critical levels, but AKI is present, a patient may proceed directly to CRRT until the period of lysis has subsided. Chemotherapy-induced rhabdomyolysis, with sustained potassium release, may also benefit from such an approach.

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related posts:

Volume disorders and fluid resuscitation Systemic light chain amyloidosis Graft-versus-host disease Paraneoplastic glomerular diseases Evaluation of a renal cyst/mass Cancer in renal transplant patients

Stay updated, free articles. Join our Telegram channel

Join