ER ribosomal-binding protein 1 regulates blood pressure and potassium homeostasis by modulating intracellular renin trafficking.

BACKGROUND: Genome-wide association studies (GWASs) have linked RRBP1 (ribosomal-binding protein 1) genetic variants to atherosclerotic cardiovascular diseases and serum lipoprotein levels. However, how RRBP1 regulates blood pressure is unknown. METHODS: To identify genetic variants associated with blood pressure, we performed a genome-wide linkage analysis with regional fine mapping in the Stanford Asia-Pacific Program for Hypertension and Insulin Resistance (SAPPHIRe) cohort. We further investigated the role of the RRBP1 gene using a transgenic mouse model and a human cell model. RESULTS: In the SAPPHIRe cohort, we discovered that genetic variants of the RRBP1 gene were associated with blood pressure variation, which was confirmed by other GWASs for blood pressure. Rrbp1- knockout (KO) mice had lower blood pressure and were more likely to die suddenly from severe hyperkalemia caused by phenotypically hyporeninemic hypoaldosteronism than wild-type controls. The survival of Rrbp1-KO mice significantly decreased under high potassium intake due to lethal hyperkalemia-induced arrhythmia and persistent hypoaldosteronism, which could be rescued by fludrocortisone. An immunohistochemical study revealed renin accumulation in the juxtaglomerular cells of Rrbp1-KO mice. In the RRBP1-knockdown Calu-6 cells, a human renin-producing cell line, transmission electron and confocal microscopy revealed that renin was primarily retained in the endoplasmic reticulum and was unable to efficiently target the Golgi apparatus for secretion. CONCLUSIONS: RRBP1 deficiency in mice caused hyporeninemic hypoaldosteronism, resulting in lower blood pressure, severe hyperkalemia, and sudden cardiac death. In juxtaglomerular cells, deficiency of RRBP1 reduced renin intracellular trafficking from ER to Golgi apparatus. RRBP1 is a brand-new regulator of blood pressure and potassium homeostasis discovered in this study.

Patiromer for the management of hyperkalemia in heart failure with reduced ejection fraction: the DIAMOND trial.

AIMS: To investigate the impact of patiromer on the serum potassium level and its ability to enable specified target doses of renin-angiotensin-aldosterone system inhibitor (RAASi) use in patients with heart failure and reduced ejection fraction (HFrEF). METHODS AND RESULTS: A total of 1642 patients with HFrEF and current or a history of RAASi-related hyperkalemia were screened and 1195 were enrolled in the run-in phase with patiromer and optimization of the RAASi therapy [≥50% recommended dose of angiotensin-converting enzyme inhibitor/angiotensin receptor blocker/angiotensin receptor-neprilysin inhibitor, and 50 mg of mineralocorticoid receptor antagonist (MRA) spironolactone or eplerenone]. Specified target doses of the RAASi therapy were achieved in 878 (84.6%) patients; 439 were randomized to patiromer and 439 to placebo. All patients, physicians, and outcome assessors were blinded to treatment assignment. The primary endpoint was between-group difference in the adjusted mean change in serum potassium. Five hierarchical secondary endpoints were assessed. At the end of treatment, the median (interquartile range) duration of follow-up was 27 (13-43) weeks, the adjusted mean change in potassium was +0.03 mmol/l in the patiromer group and +0.13 mmol/l in the placebo group [difference in the adjusted mean change between patiromer and placebo: -0.10 mmol/l (95% confidence interval, CI -0.13, 0.07); P < 0.001]. Risk of hyperkalemia >5.5 mmol/l [hazard ratio (HR) 0.63; 95% CI 0.45, 0.87; P = 0.006), reduction of MRA dose (HR 0.62; 95% CI 0.45, 0.87; P = 0.006), and total adjusted hyperkalemia events/100 person-years (77.7 vs. 118.2; HR 0.66; 95% CI 0.53, 0.81; P < 0.001) were lower with patiromer. Hyperkalemia-related morbidity-adjusted events (win ratio 1.53, P < 0.001) and total RAASi use score (win ratio 1.25, P = 0.048) favored the patiromer arm. Adverse events were similar between groups. CONCLUSION: Concurrent use of patiromer and high-dose MRAs reduces the risk of recurrent hyperkalemia (ClinicalTrials.gov: NCT03888066).

Current Management of Hyperkalemia in Non-Dialysis CKD: Longitudinal Study of Patients Receiving Stable Nephrology Care.

BACKGROUND: No study has explored the limitations of current long-term management of hyperkalemia (HK) in outpatient CKD clinics. METHODS: We evaluated the association between current therapeutic options and control of serum K (sK) during 12-month follow up in ND-CKD patients stratified in four groups by HK (sK ≥ 5.0 mEq/L) at baseline and month 12: Absent (no-no), Resolving (yes-no), New Onset (no-yes), Persistent (yes-yes). RESULTS: We studied 562 patients (age 66.2 ± 14.5 y; 61% males; eGFR 39.8 ± 21.8 mL/min/1.73 m2, RAASI 76.2%). HK was "absent" in 50.7%, "resolving" in 15.6%, "new onset" in 16.6%, and "persistent" in 17.1%. Twenty-four hour urinary measurements testified adherence to nutritional recommendations in the four groups at either visit. We detected increased prescription from baseline to month 12 of bicarbonate supplements (from 5.0 to 14.1%, p < 0.0001), K-binders (from 2.0 to 7.7%, p < 0.0001), and non-K sparing diuretics (from 34.3 to 41.5%, p < 0.001); these changes were consistent across groups. Similar results were obtained when using higher sK level (≥5.5 mEq/L) to stratify patients. Mixed-effects regression analysis showed that higher sK over time was associated with eGFR < 60, diabetes, lower serum bicarbonate, lower use of non-K sparing diuretics, bicarbonate supplementation, and K-binder use. Treatment-by-time interaction showed that sK decreased in HK patients given bicarbonate (p = 0.003) and K-binders (p = 0.005). CONCLUSIONS: This observational study discloses that one-third of ND-CKD patients under nephrology care remain with or develop HK during a 12-month period despite low K intake and increased use of sK-lowering drugs.

Abdominal Wall Pain: A Common Clinical Problem.

Abdominal wall pain (AWP) is a common and underrecognized cause of chronic abdominal pain. The etiology of AWP varies. History and physical examination are critical to an accurate diagnosis of AWP. Trigger point injection using either a corticosteroid, a local anesthetic, or a combination of both often gives relief of pain and is of diagnostic and therapeutic value. Increased awareness of AWP as a cause of chronic, nonvisceral abdominal pain can prevent fruitless searches for intra-abdominal pathology and reduce medical costs.

Dyskalemia in Chronic Kidney Disease: How Concerned Should We Be?

CONTEXT: The widespread use of diuretics, potassium supplements, and medications that block renin angiotensin system puts the chronic kidney disease (CKD) population at high risk for dyskalemia, both hyperkalemia and hypokalemia. The optimal potassium level in a CKD patient is unknown. Subject of review: Two recent studies found conflicting results on the association of dyskalemia with outcomes. The Renal Research Institute CKD study [Clin J Am Soc Nephrol 2010; 5: 762-769] found increased mortality and incidence of end-stage renal disease (ESRD) with mild to moderate hypokalemia, whereas hyperkalemia was not significantly associated, compared to eukalemia. On the other hand, the Multi-Ethnic Study of Atherosclerosis (MESA)/Cardiovascular Health Study [Clin J Am Soc Nephrol 2017; 12: 245-252] showed both cardiovascular and noncardiovascular mortality to be higher with hyperkalemic patients, whereas associations with hypokalemic patients were statistically nonsignificant. Second opinion: If mild hypo- or hyperkalemia is associated with adverse outcomes, is it related to the hyperkalemia per se or to conditions associated with dyskalemia, such as kidney disease or cardiovascular disease? We interpret these articles in the context of criteria to support causality in epidemiologic studies. The cardiovascular effects of dyskalemia is well described and there is biological plausibility for increased cardiovascular mortality but the association of increased non-cardiovascular mortality with dyskalemia has little mechanistic basis. The explanation for a causal association of dyskalemia with ESRD is not adequate. Based on current evidence, targeting a potassium level of 4-5 mmol/L can be considered safe.

Hyperkalaemia in people with diabetes: occurrence, risk factors and outcomes in a Danish population-based cohort study.

AIMS: To examine the incidence, risk factors and clinical outcomes of hyperkalaemia in people with diabetes in a real-world setting. METHODS: Using Danish health registries, we identified a population-based cohort of people with first-time drug-treated diabetes, in the period 2000-2012. First, the cumulative incidence of hyperkalaemia, defined as first blood test with potassium level >5.0 mmol/l after diabetes treatment initiation, was ascertained. Second, in a case-control analysis, risk factors were compared in people with vs without hyperkalaemia. Third, clinical outcomes were assessed among individuals with hyperkalaemia in a before-after analysis, and among people with and without hyperkalaemia in a matched cohort analysis. RESULTS: Of 68 601 individuals with diabetes (median age 62 years, 47% women), 16% experienced hyperkalaemia (incidence rate 40 per 1000 person-years) during a mean follow-up of 4.1 years. People who developed hyperkalaemia had a higher prevalence of chronic kidney disease [prevalence ratio 1.74 (95% CI 1.68-1.81)], heart failure [prevalence ratio 2.35 (95% CI 2.18-2.54)], use of angiotensin-converting enzyme inhibitors [prevalence ratio 1.24 (95% CI 1.20-1.28)], use of spironolactone [prevalence ratio 2.68 (95% CI 2.48-2.88)] and potassium supplements [prevalence ratio 1.59 (95% CI 1.52-1.67)]. In people with diabetes who developed hyperkalaemia, 31% were acutely hospitalized within 6 months before hyperkalaemia, increasing to 50% 6 months after hyperkalaemia [before-after risk ratio 1.67 (95% CI 1.61-1.72)]. The 6-month mortality rate after hyperkalaemia was 20%. Compared with matched individuals without hyperkalaemia, the hazard ratio for death was 6.47 (95% CI 5.81-7.21). CONCLUSIONS: One in six newly diagnosed people with diabetes experienced a hyperkalaemic event, which was associated with severe clinical outcomes and death.

High Dose Oral Furosemide with Salt Ingestion in the Treatment of Refractory Ascites of Liver Cirrhosis.

PURPOSE: We aimed to evaluate and compare the efficacy and safety of high-dose furosemide+salt orally by comparing HSS+ furosemide (i.v.) and repeated paracentesis in patients with RA. METHODS: This was a prospective study of 78 cirrhotic patients with RA, randomized into three groups: Group A (n= 25) i.v. furosemide (200-300 mg bid) and 3% hypotonic saline solution (HSS) (once or twice a day); Group B (n= 26) oral furosemide tablets (360-520 mg bid) and salt (2.5 g bid); and, Group C (n= 27) repeated large-volume-paracentesis (RLVP) with albumin infusion. Patients without hyperkalemia were administrated 100 mg of spironolactone/day. During the follow-up; INR, creatinine, and total bilirubin levels were measured to determine the change in MELD (model of end stage liver disease) score. RESULTS: Hepatic encephalopathy (HE), severe episodes of spontaneous bacterial peritonitis (SBP) and pleural effusions (PE) occurred more frequently in Group C. Improvement in Child-Pugh and MELD score was better in Group A and B than Group C. In Group B, improvements were seen in the Child-Pugh and MELD score, reduction in body weight, duration and number of hospitalization. In Groups A and B, remarkable increases in diuresis were observed (706±116 to 2425±633 mL and 691±111 to 2405±772 mL) and serum sodium levels also improved. HE and SBP were occurred more often in group C (p<0.002). Hospitalization decreased significantly in Group B (p<0.001). There was no significant difference in survival among groups. CONCLUSION: High dose oral furosemide with salt ingestion may be an alternative, effective, safe and well-tolerated method of therapy for RA.

Acute kidney injury from cherry concentrate in a patient with CKD.

Nutraceuticals are supplements and medical foods that offer numerous health benefits. However, these substances may have adverse effects on multiple organ systems, leading to significant morbidity. I present a patient with chronic kidney disease who experienced hemodynamically mediated acute kidney injury and hyperkalemia after daily consumption of cherry concentrate. The method of injury was most likely cyclooxygenase inhibition by the compounds in cherries that mimic the mechanism of action of nonsteroidal anti-inflammatory medications. Ceasing cherry concentrate consumption led to improvements in both the patient's hyperkalemia and kidney injury. Physicians should be aware of the potentially harmful side effects of cherry concentrate and approach the use of cherry extract or concentrate with caution in patients with underlying kidney disease.

Pretreatment of formula or expressed breast milk with sodium polystyrene sulfonate (Kayexalate(®)) as a treatment for hyperkalemia in infants with acute or chronic renal insufficiency.

OBJECTIVE: To evaluate the effect on serum potassium of treating infant formula or expressed breast milk (EBM) with sodium polystyrene sulfonate (SPS) before patient consumption. DESIGN AND SETTING: Retrospective cohort study of patients at Seattle Children's Hospital who received SPS-treated formula or EBM. SUBJECTS AND INTERVENTION: Thirteen patients less than 2 years of age with a diagnosis of hyperkalemia and acute kidney injury or chronic kidney disease that had received formula or EBM pretreated with SPS between September 2009 and May 2012 were identified. Hyperkalemia was defined as a serum potassium concentration greater than 5.5 mEq/L. MAIN OUTCOME MEASURE: The primary endpoint was the mean change in serum potassium 48 hours after receiving pretreated formula or EBM. Serum potassium levels before and after patient consumption were averaged and compared using a paired t test. RESULTS: Pretreatment of formula or EBM with SPS resulted in a 24% decrease in serum potassium levels (6.3 mEq/L to 4.8 mEq/L; P < .0001). There was a significant difference in before and after calcium and creatinine levels (P < .05), and no significant differences in blood urea nitrogen, sodium, magnesium, phosphorus, chloride, or bicarbonate levels. CONCLUSION: Pretreatment of formula or EBM with SPS before consumption is an effective treatment for hyperkalemia in infants. Caution needs to be taken in patients who have sodium restrictions because the exchange for potassium produces a sodium-rich formula.

Intestinal Necrosis Associated with Orally Administered Calcium Polystyrene Sulfonate Without Sorbitol.

OBJECTIVE: To describe a case of extensive intestinal necrosis with oral intake of calcium polystyrene sulfonate without sorbitol. CASE SUMMARY: A 73-year-old woman was admitted to the emergency department with abdominal pain. Abdominal computed tomography (CT) scan showed widespread dilatation of the bowel. The diagnosis of acute colonic pseudoobstruction was made. On day 3, her serum potassium level rose to 5.6 mEq/L. It was treated with hydrocortisone 100 mg/day and calcium polystyrene sulfonate 15 g/day via nasogastric tube from day 3 to day 6. On day 6, the severe abdominal pain recurred, with abdominal tenderness. CT scan showed pneumoperitoneum and peritoneal effusion. At surgery, 2 lenticular jejunal perforations and an ischemic cecum were found. Microscopic findings indicated that the transmural abscess contained massive inflammatory infiltrate and the cecal mucosa showed ulceration and inflammation with a fibrinous and purulent coating. Small gray-purple or blue angulated crystals were embedded in the cecal and most of the jejunal mucosal ulcers. On day 19, the patient died of multiple organ failure after her third laparotomy. DISCUSSION: Ion-exchanging resins are given orally or by retention enema for the treatment of hyperkalemia. The most commonly used and best-established resin is sodium polystyrene sulfonate. However, it is known to promote colonic necrosis when sorbitol is also given or especially in patients with renal failure or postoperative ileus. Calcium polystyrene sulfonate is another ion-exchange resin. There are few reports of adverse effects in the literature. Our case is interesting for 2 reasons: the resin given was calcium polystyrene sulfonate and sorbitol was not used. CONCLUSIONS: Like sodium polystyrene sulfonate, calcium polystyrene sulfonate is an ion-exchanging resin that can promote bowel necrosis. We believe that it should not be used with sorbitol or when bowel transit time is slowed.

Hypertension of Kcnmb1-/- is linked to deficient K secretion and aldosteronism.

Mice lacking the beta1-subunit (gene, Kcnmb1; protein, BK-beta1) of the large Ca-activated K channel (BK) are hypertensive. This phenotype is thought to result from diminished BK currents in vascular smooth muscle where BK-beta1 is an ancillary subunit. However, the beta1-subunit is also expressed in the renal connecting tubule (CNT), a segment of the aldosterone-sensitive distal nephron, where it associates with BK and facilitates K secretion. Because of the correlation between certain forms of hypertension and renal defects, particularly in the distal nephron, it was determined whether the hypertension of Kcnmb1(-/-) has a renal origin. We found that Kcnmb1(-/-) are hypertensive, volume expanded, and have reduced urinary K and Na clearances. These conditions are exacerbated when the animals are fed a high K diet (5% K; HK). Supplementing HK-fed Kcnmb1(-/-) with eplerenone (mineralocorticoid receptor antagonist) corrected the fluid imbalance and more than 70% of the hypertension. Finally, plasma [aldo] was elevated in Kcnmb1(-/-) under basal conditions (control diet, 0.6% K) and increased significantly more than wild type when fed the HK diet. We conclude that the majority of the hypertension of Kcnmb1(-/-) is due to aldosteronism, resulting from renal potassium retention and hyperkalemia.

Severe muscle weakness due to hyperkalemia.

Hyperkalemia is a commonly encountered electrolyte disturbance in patients with renal insufficiency. It develops very rapidly when potassium is supplemented while a patient is on a potassium-sparing diuretic. Most often it remains asymptomatic and manifests in the form of electrocardiographic changes. Muscle weakness and paralysis although described is seldom observed in clinical practice. We report one such case.

Penile calciphylaxis.

Calciphylaxis is an uncommon condition usually seen in patients with end-stage renal disease. The typical features include violaceous skin lesions overlying painful, indurated, subcutaneous nodules. Necrosis and nonhealing ulcers, with secondary gangrene, sepsis, and death frequently follow. The outpatient hemodialysis population has a reported calciphylaxis prevalence of 1% to 4.1%; however, published studies contain only a few case reports of penile calciphylaxis. The urologic presentation consists primarily of penile gangrene. A description of our patient, the underlying pathologic features, a review of the relevant published studies, and the possible predisposing conditions are included.

Complex ventricular arrhythmia induced by overuse of potassium supplementation in a young male football player. Case report.

People practising regular physical activity usually drink hydrosaline beverages. In this study is reported the case of a young football player suffering from premature ventricular beats. He used to take regularly an hydrosaline supplementation which gave him a daily intake of potassium of about 5 g. A stress test on a cycle ergometer showed many monomorphus premature ventricular beats which disappeared when the heart rate was higher than 110 beats/min. Moreover, 3629 polimorphus premature ventricular beats were recorded during a 24 hr ECG monitoring. At the time of the first examination, the plasma potassium concentration was 7,8 mEq x l(-1). The football player was then suspended from practicing sport and he was asked to stop his intake of potassium. The clinical examination was repeated after 3 and 6 months and no ventricular arrhythmias were observed during the stress test as well as during the 24 hours ECG monitoring. The plasma potassium concentration was normal again. The present case report is an example of how the misuse of saline supplementations could result in hyperkalemia and how this condition may lead to ventricular arrhythmias.

[Malignant arrhythmias caused by hyperkalemia: a new area of drug-induced electrolyte abnormalities]. / Hyperkalaemia okozta malignus ritmuszavarok: a gyógyszer indukálta elektrolitzavarok új korszaka.

INTRODUCTION: High dose of angiotensin converting enzyme inhibitor is indicated in the treatment of heart failure and it is part of the treatment in the patients suffering from diabetes mellitus and nephropathy. The patients with preexisting renal insufficiency could have slowly elevated serum potassium level treated by angiotensin converting enzyme inhibitor. PATIENTS: Seven acute admitted cases is presented with severe hyperkalaemia and life threatening arrhythmias caused by ACEI administration. Wide QRS accelerated rhythm was detected in two cases and bradyarrhythmias in five cases. Two patients died among the bradyarrhythmias. CONCLUSIONS: The authors call the attention of danger of high dose angiotensin converting enzyme inhibitor in patients with preexisting renal insufficiency and concomittant drugs elevating serum potassium level.

Life threatening hyperkalemia and acidosis secondary to trimethoprim-sulfamethoxazole treatment.

We present a 77-year-old male with moderate chronic renal insufficiency from diabetic nephropathy who developed severe metabolic acidosis and life threatening hyperkalemia on treatment with regular dose of trimethoprim-sulfamethoxazole (TMP-SMZ) for urinary tract infection. The metabolic acidosis and hyperkalemia resolved upon appropriate medical intervention and discontinuation of TMP-SMZ. While hyperkalemia has commonly been reported with high dose of TMP-SMZ, severe metabolic acidosis is quite uncommon with regular dose TMP-SMZ. We emphasize that patients with renal tubular acidosis (RTA), renal insufficiency, aldosterone deficiency, old age with reduced renal mass and function, and angiotensin converting enzyme (ACE)-inhibitor therapy are at high risk of developing these severe and potentially life threatening complications.

Long-term myocardial preservation: effects of hyperkalemia, sodium channel, and Na/K/2Cl cotransport inhibition on extracellular potassium accumulation during hypothermic storage.

OBJECTIVES: We previously demonstrated improved myocardial preservation with polarized (tetrodotoxin-induced), compared with depolarized (hyperkalemia-induced), arrest and hypothermic storage. This study was undertaken to determine whether polarized arrest reduced ionic imbalance during ischemic storage and whether this was influenced by Na+/K +/2Cl- cotransport inhibition. METHODS: We used the isolated crystalloid perfused working rat heart preparation (1) to measure extracellular K+ accumulation (using a K+-sensitive intramyocardial electrode) during ischemic (control), depolarized (K+ 16 mmol/L), and polarized (tetrodotoxin, 22 micromol/L) arrest and hypothermic (7.5 degrees C) storage (5 hours), (2) to determine dose-dependent (0.1, 1.0, 10 and 100 micromol/L) effects of the Na +/K+/2Cl- cotransport inhibitor, furosemide, on extracellular K+ accumulation during polarized arrest and 7.5 degrees C storage, and (3) to correlate extracellular K+ accumulation to postischemic recovery of cardiac function. RESULTS: Characteristic triphasic profiles of extracellular K+ accumulation were observed in control and depolarized arrested hearts; a significantly attenuated profile with polarized arrested hearts demonstrated reduced extracellular K+ accumulation, correlating with higher postischemic function (recovery of aortic flow was 54% +/-4% [P =.01] compared with 39% +/-3% and 32% +/-3% in depolarized and control hearts, respectively). Furosemide (0.1, 1.0, 10, and 100 micromol/L) modified extracellular K+ accumulation by -18%, -38%, -0.2%, and +9%, respectively, after 30 minutes and by -4%, -27%, +31%, and +42%, respectively, after 5 hours of polarized storage. Recovery of aortic flow was 53% +/-4% (polarized arrest alone), 56% +/-8%, 70% +/-2% (P =.04 vs control), 69% +/-4% (P =.04 vs control), and 65% +/-3% ( P =. 04 vs control), respectively. CONCLUSIONS: Polarized arrest was associated with a reduced ionic imbalance (demonstrated by reduced extracellular K+ accumulation) and improved recovery of cardiac function. Further attenuation of extracellular K + accumulation (by furosemide) resulted in additional recovery.

Un caso atípico de abdomen agudo / Atipical case of acute abdomen

Introducción: El potasio es el ión más importante en el funcionamiento de las células excitables, la hiperkalemia se relaciona con efectos peligrosos sobre miocardio, músculo liso y nervios periféricos. A pesar de la clara asociación fisiopatológica entre el aumento del potasio y el íleo paralítico, no se han hallado casos que mencionen al abdomen agudo como forma de presentación en la búsqueda bibliográfica por Medline de los últimos diez años. Se presenta por tanto un caso en el cual el motivo de consulta fue dolor abdominal. Presentación: Paciente de sexo femenino, 83 años, consulta por dolor abdominal muy intenso asociado a náuseas y oliguria de 24 hs de evolución. Antecedentes: tromboembolismo de pulmón a repetición a pesar de estar anticoagulada de forma suficiente, hipertensión pulmonar, fibrilación auricular, medicada con furosemida, espironolactoma, digoxina, acenocumarol. Examen físico: desasosegada, taquipneica, soplo de regurgitación tricúspidea, abdomen doloroso, sin ruidos hidroaéreos. Urea: 108 mg por ciento, creatinina: 1,91 mg/dl, K: 6,8 meq, Ph: 7,52, Po2: 142, PCo2 35, COH3 29,9. ECG: ritmo nodal. Colon por enema: dolicocolon. Ecografía abdominal y endoscopía esófago-gástrica normales. Se trata con soluciones polarizantes, cediendo el dolor abdominal y retornando el ritmo cardíaco a fibrilación auricular, recupera el ritmo diurético y normaliza urea y creatinina. Conclusiones: 1) Esta hiperkalemia sin fallo renal crónico previo fue multifactorial. a- Uso prolongado de espironolactona en paciente deshidratada con escaso aporte de Na. b- Seudohipoaldosteronismo. c- Alcalosis mixta. 2) Debido a la acción del potasio sobre las células excitables, la hiperkalemia puede provocar íleo paralítico y presentarse como abdomen agudo sobre todo en pacientes polimedicados (AU)