Severe acute kidney injury due to oxalate crystal induced severe interstitial nephritis: A case report.

BACKGROUND: Acute kidney injury (AKI) due to interstitial nephritis is a known condition primarily attributed to various medications. While medication-induced interstitial nephritis is common, occurrences due to non-pharmacological factors are rare. This report presents a case of severe AKI triggered by intratubular oxalate crystal deposition, leading to interstitial nephritis. The aim is to outline the case and its management, emphasizing the significance of recognizing uncommon causes of interstitial nephritis. CASE SUMMARY: A 71-year-old female presented with stroke-like symptoms, including weakness, speech difficulties, and cognitive impairment. Chronic hypertension had been managed with hydrochlorothiazide (HCTZ) for over two decades. Upon admission, severe hypokalemia and AKI were noted, prompting discontinuation of HCTZ and initiation of prednisolone for acute interstitial nephritis. Further investigations, including kidney biopsy, confirmed severe acute interstitial nephritis with oxalate crystal deposits as the underlying cause. Despite treatment, initial renal function showed minimal improvement. However, with prednisolone therapy and supportive measures, her condition gradually improved, highlighting the importance of comprehensive management. CONCLUSION: This case underscores the importance of a thorough diagnostic approach in identifying and addressing uncommon causes of interstitial nephritis. The occurrence of interstitial nephritis due to oxalate crystal deposition, especially without typical risk factors, emphasizes the need for vigilance in clinical practice.

Hepatitis C Presenting Like Endocarditis in a Young Patient With Substance Use Disorder: A Case Report.

This case report details a 21-year-old male patient who initially presented with endocarditis-like symptoms but ultimately had hepatitis C in the setting of substance use disorder. It highlights the value of prompt diagnosis and effective treatment. He had a medical history of chronic heroin use over two years and presented inconsistently to the emergency department with generalized body aches. He had generalized body pain and right upper and lower quadrant abdominal pain. He had been unable to tolerate any oral intake and had been vomiting after every meal for the last three weeks. Physical examination was significant only for large, ovoid, erythematous nodules on the left dorsal foot, blanching and slightly painful to touch; diffuse scabs and sores on extremities; and nodules on dorsal interphalangeal joints on the left hand. Urine drug screen was noted to be positive for cannabinoids, methamphetamines, and opioids. The initial electrocardiogram did not show typical T wave flattening changes for hypokalemia. Transthoracic echocardiogram ruled out infective endocarditis, with no valvular vegetation. He was ultimately found to be hepatitis C virus antibody positive. This case illustrates the importance of keeping a wide differential in mind. The patient had hepatitis C despite being asymptomatic throughout presentation-keeping. The patient's history of heroin use was critical while ordering testing.

Convergence of Crisis: A Case Report of Diabetic Ketoacidosis Masking an Impending Thyroid Storm and Periodic Paralysis.

Diabetic ketoacidosis (DKA) is an extreme complication of diabetes mellitus characterized by hyperglycemia, metabolic acidosis, and ketonemia. Thyroid storm, a potentially life-threatening manifestation of thyrotoxicosis, presents with a multitude of symptoms, including hyperthermia, tachycardia, and altered mental status. Periodic paralysis can be precipitated by different metabolic disturbances, including thyrotoxicosis, and may lead to extreme episodes of muscle weakness and paralysis. We present a case of a 41-year-old female with a history of type 1 diabetes mellitus and hyperthyroidism, who presented with DKA complicated by an impending thyroid storm and likely periodic paralysis exacerbated due to hypokalemia. Prompt recognition and aggressive management of each component of this triad were essential for a positive patient outcome. This case highlights the importance of a broad and comprehensive approach to managing complex metabolic emergencies, particularly in patients with multiple comorbidities. Our patient presented to the emergency department with symptoms of severe vomiting, shortness of breath, and altered mental status. Laboratory investigations revealed metabolic derangements consistent with DKA, alongside impending thyrotoxicosis and hypokalemia-induced periodic paralysis. Management involved aggressive fluid resuscitation, insulin therapy, anti-thyroid medications, and potassium supplementation, with a multidisciplinary approach to stabilize the patient's condition.

First Diagnosis of Gitelman Syndrome During Pregnancy in an Adolescent Female: A Case Report.

Gitelman syndrome (GS) is an inherited somatic recessive disorder characterized by hypokalemic metabolic alkalosis, accompanied by hypocalciuria and hypermagnesuria. It usually presents in late childhood or young adults with muscle weakness, tetany, or convulsions. Limited information is available in the literature regarding the proper management of this syndrome during pregnancy, as well as its effects on both the mother and the child. We herein present the case of a 16-year-old primigravida who was admitted to the emergency department with chief complaints of abdominal pain, weakness, and vomiting for the past three days during the 12th week of gestation. Routine blood investigations revealed hypokalemia and hypomagnesemia, and electrocardiography (ECG) showed ST-segment depressions. Further evaluation was performed due to persistent hypokalemia, and metabolic alkalosis, hypocalciuria, and hyperaldosteronism were found. Hence, a clinical diagnosis of GS took place. The pregnancy progressed smoothly without complications; potassium levels remained consistently below normal, requiring supplementation three times during pregnancy. Pregnant women with GS should be reported due to the rarity of cases, aiming to establish a standardized approach for monitoring and management.

Prevalence, predictive factors, and outcomes of refeeding syndrome among medically critically ill patients: A retrospective cohort study.

BACKGROUND: Refeeding syndrome (RFS) is a life-threatening metabolic derangement occurring when nutrition is reintroduced after prolonged starvation. Limited data exist regarding RFS prevalence, risk factors, and outcome, particularly in critically ill patients. METHODS: A retrospective cohort study was conducted in a medical intensive care unit from June 2018 to August 2020. RFS diagnostic criteria from the National Institute for Health and Care Excellence (NICE) and the American Society for Parenteral and Enteral Nutrition (ASPEN) were used. The primary outcome was 30-day mortality. RESULTS: Among 216 patients, RFS was diagnosed in 22.7% and 27.3% of patients per the NICE and ASPEN criteria, respectively. There was no significant difference in 30-day mortality between patients with and without RFS (22/59 [37.3%] vs 53/157 [33.8%]; P = 0.627). Independent predictors of RFS were malignancy (odds ratio [OR] = 2.09; 95% CI = 1.06-4.15; P = 0.035), septic shock (OR = 2.26; 95% CI = 1.17-4.39; P = 0.016), and high NICE RFS risk classification (OR = 2.52; 95% CI = 1.20-5.31; P = 0.015). Factors associated with reduced RFS risk were Sequential Organ Failure Assessment (SOFA) scores >12 (OR = 0.45; 95% CI = 0.23-0.88; P = 0.020) and high-dose vasopressor treatment (OR = 0.34; 95% CI = 0.14-0.79; P = 0.012). CONCLUSION: RFS affected one-fourth of the critically ill patients but did not significantly impact 30-day mortality. Malignancy, septic shock, and high NICE RFS risk classification were positively associated with RFS, whereas high SOFA scores and extensive vasopressor use were linked to decreased risk.

HELIX Syndrome, a Claudinopathy with Relevant Dermatological Manifestations: Report of Two New Cases.

HELIX syndrome (Hypohidrosis-Electrolyte disturbances-hypoLacrimia-Ichthyosis-Xerostomia) (MIM#617671) (ORPHA:528105), described in 2017, is due to an abnormal claudin 10 b protein, secondary to pathogenic CLDN10 variants. So far, only ten families have been described. We aim to describe the phenotype in the first Spanish family identified, highlight the skin anomalies as an important clue, and expand the genotypic spectrum. Two adult brothers from consanguineous parents with suspected ectodermal dysplasia (ED) since early childhood were re-evaluated. A comprehensive phenotypic exam and an aCGH + SNP4 × 180 K microarray followed by Sanger sequencing of the CLDN10 gene were performed. They presented hypohidrosis, xerosis, mild ichthyosis, plantar keratosis, palm hyperlinearity, alacrima, and xerostomia. In adulthood, they also developed a salt-losing nephropathy with hypokalemia and hypermagnesemia. The molecular study in both patients revealed a novel pathogenic homozygous deletion of 8 nucleotides in exon 2 of the CLDN10 gene [CLDN10 (NM_0006984.4): c.322_329delGGCTCCGA, p.Gly108fs*] leading to a premature truncation of the protein. Both parents were heterozygous carriers. Hypohidrosis, ichthyosis, and plantar keratosis associated with alacrima and xerostomia should raise suspicion for HELIX syndrome, which also includes nephropathy and electrolyte disturbances in adults. Given the potential for ED misdiagnosis in infancy, it is important to include the CLDN10 gene in a specific genodermatosis next-generation sequencing (NGS) panel to provide early diagnosis, accurate management, and genetic counseling.

Case report: thyrotoxic periodic paralysis, an unusual cause of hypokalemia.

Introduction: Thyrotoxic periodic paralysis (TPP) is a type of hypokalemic periodic paralysis that is caused by an underlying thyrotoxicosis. It is a rare cause of hypokalemia due to intracellular potassium shift, causing acute muscle weakness.Case presentation: We present a case of a 19-year-old male of Thai descent with acute proximal symmetric lower limb weakness. The combination of these symptoms with profound hypokalemia, rapid recovery after normalization of serum potassium, and evidence of hyperthyroidism led to the diagnosis of thyrotoxic periodic paralysis, in this case due to an underlying Graves' disease.Conclusion: Clinicians should consider the diagnosis of TPP when a patient presents with the triad of acute paresis, profound hypokalemia and hyperthyroidism.

A rare cause of hypokalemia.

Hypokalemia is a common electrolyte derangement seen in the inpatient setting, often with multiple plausible explanations. However, for patients with nonobvious causes, obtaining a more thorough history, including dietary history, can yield valuable insight and clues to guide clinicians in their evaluation.

Intriguing association between type 1 diabetes mellitus, Gitelman syndrome and Cacci-Ricci disease: Triad of rare diseases: A case report.

We report the case of a patient who exhibits a concurrent diagnosis of type 1 diabetes mellitus, Gitelman syndrome and Cacci-Ricci disease. A 27-year-old male patient was diagnosed with Gitelman syndrome at the age of 3 years. Fourteen years later, he developed an autoantibody-negative type 1 diabetes mellitus. Cacci-Ricci's disease was revealed by terminal hematuria and considered in view of the appearance found on the computed tomography (CT) scan. The finger-prick blood glucose level was 6 g/dl with no acetonuria. Creatinine clearance was 60 ml/min. Thyroid function tests were normal. Calcium, phosphorus and parathormone (PTH) levels were normal. Discussion: Gitelman syndrome is a rare disorder. The association between Gitelman syndrome and type 1 diabetes mellitus has been reported in the literature in two patients. Authors have investigated the association between Gitelman syndrome and type 2 diabetes mellitus. Several pathophysiological explanations have been put forward. Cacci-ricci disease is a rare, benign congenital anomaly. No association between type 1 diabetes mellitus, Gitelman syndrome and Cacci-Ricci disease has been reported in the literature. To our knowledge, this is the first case described in the literature.

Pseudonormokalemia case report - What does it mean to have normal blood potassium?

This case report describes a case of pseudonormokalemia, true hypokalemia. Often, only laboratory values outside the normal range gain attention and false normal results are at risk of not being noticed. However, a disease state may be masked by another pathological process. Here, a 50-year old male was admitted to the Department of Internal Medicine due to sepsis from a dental infection. Initially, serum potassium measurement revealed a normal value of 4 mmol/L (reference interval 3.8-5.1 mmol/L). Thrombocyte number was above 500x109/L. Due to our policy to recommend a repeated measurement of potassium in whole blood or heparin plasma if a patient has thrombocytosis, pseudonormokalemia was identified because the heparin plasma potassium value was only 2.9 mmol/L (reference interval 3.5-4.8 mmol/L). The physiological difference between serum and plasma concentration is no more than 0.3 mmol/L. In this case, potassium concentration were falsely elevated in the serum sample, probably caused by the high number of platelets releasing potassium during clotting. Interpretative comments in patients with thrombocytosis over 500x109/L recommending plasma potassium measurement are helpful. The best way to eliminate pseudohyperkalemia and pseudonormokalemia phenomena caused by thrombocytosis is to completely change towards heparin plasma as the standard material.

Etomidate-induced hypokalemia in electronic cigarette users: two case reports and literature review.

Hypokalemia is a common clinical condition that can lead to muscle weakness, difficulty breathing, malignant arrhythmias, and even death. This report describes two cases of severe hypokalemia resulting from the use of electronic cigarettes containing etomidate, both accompanied by varying degrees of adrenal hyperplasia. In both cases, the patients were admitted to the hospital with lower limb weakness and difficulty walking. Relevant examinations revealed low blood potassium, low cortisol, high adrenocorticotropic hormone, low renin, and low aldosterone levels in the patients, with Case 2 also having significant hypertension. In both cases, adrenal CT scans showed thickening of the adrenal glands. After the delivery of potassium supplementation in both cases, blood potassium levels gradually returned to normal and muscle strength gradually improved. The case reports are followed by a review of the literature on etomidate and its related mechanisms of action with discussion of its association with hypokalemia.

Hyperinsulinemic State and Hypokalemic Quadriparesis in Tropical Fever: Is There a Link?

It is rare for quadriparesis to manifest as a symptom of tropical illnesses. With a history of only one fever episode one week prior, our patient, a 48-year-old male with obesity and prediabetes, who was also known to have ankylosing spondylitis, presented with acute onset flaccid quadriparesis. He did not exhibit any additional symptoms of dengue, such as bleeding tendencies, petechial rashes, thrombocytopenia, or febrile episodes. Upon examination, it was discovered that he had extremely low serum potassium levels and was dengue non-specific antigen 1 (NS1) positive. His hyperinsulinemia, as seen by elevated C peptide levels, most likely caused a transcellular shift that was then triggered by the dengue infection, leading to hypokalemic paralysis.

Impaired distal renal potassium handling in streptozotocin-induced diabetic mice.

Diabetes is closely associated with K+ disturbances during disease progression and treatment. However, it remains unclear whether K+ imbalance occurs in diabetes with normal kidney function. In this study, we examined the effects of dietary K+ intake on systemic K+ balance and renal K+ handling in streptozotocin (STZ)-induced diabetic mice. The control and STZ mice were fed low or high K+ diet for 7 days to investigate the role of dietary K+ intake in renal K+ excretion and K+ homeostasis and to explore the underlying mechanism by evaluating K+ secretion-related transport proteins in distal nephrons. K+-deficient diet caused excessive urinary K+ loss, decreased daily K+ balance, and led to severe hypokalemia in STZ mice compared with control mice. In contrast, STZ mice showed an increased daily K+ balance and elevated plasma K+ level under K+-loading conditions. Dysregulation of the NaCl cotransporter (NCC), epithelial Na+ channel (ENaC), and renal outer medullary K+ channel (ROMK) was observed in diabetic mice fed either low or high K+ diet. Moreover, amiloride treatment reduced urinary K+ excretion and corrected hypokalemia in K+-restricted STZ mice. On the other hand, inhibition of SGLT2 by dapagliflozin promoted urinary K+ excretion and normalized plasma K+ levels in K+-supplemented STZ mice, at least partly by increasing ENaC activity. We conclude that STZ mice exhibited abnormal K+ balance and impaired renal K+ handling under either low or high K+ diet, which could be primarily attributed to the dysfunction of ENaC-dependent renal K+ excretion pathway, despite the possible role of NCC.NEW & NOTEWORTHY Neither low dietary K+ intake nor high dietary K+ intake effectively modulates renal K+ excretion and K+ homeostasis in STZ mice, which is closely related to the abnormality of ENaC expression and activity. SGLT2 inhibitor increases urinary K+ excretion and reduces plasma K+ level in STZ mice under high dietary K+ intake, an effect that may be partly due to the upregulation of ENaC activity.

The Silent Threat of Hypokalemia after High Voltage Electrical Injuries: A Case Study and Review of the Literature.

High-voltage electrical injuries, especially from lightning strikes, can cause life-threatening complications due to extreme temperature and voltage exposure. While burns and cardiac complications have been widely described, the documentation of metabolic imbalances, particularly hypokalemia, has not been as prevalent. This report focuses on a patient with profound transient hypokalemia following a lightning strike, alongside a review of three similar cases of transient hypokalemia from the literature. Our patient, a previously healthy young man, was struck by lightning and subsequently suffered transient hypokalemia with lower extremity sensory changes, which resolved after the normalization of serum potassium levels. While the exact underlying mechanisms of transient hypokalemia following high-voltage electrical injuries are unknown, we propose a multifactorial mechanism, which includes massive intracellular shifts of potassium due to elevated epinephrine levels and the prevention of potassium efflux through the electrical disruption of voltage-gated potassium channels. Our report underscores the importance of recognizing hypokalemia in patients with high-voltage electrical injuries and contributes to the understanding of the complex mechanisms involved. Further research is necessary to understand the connection between cellular changes induced by high-voltage exposure and their effects on metabolism, particularly in relation to hypokalemia.

Hypokalemic paralysis following intramuscular betamethasone injection: A case report and review of literature.

Acute neuromuscular paralysis is a relatively common condition in emergency rooms (ERs). They can be caused by several reasons, including adverse drug reactions. Betamethasone is a glucocorticoid commonly used for various conditions, such as allergic conditions. One of the rare but known side effects of glucocorticoids is hypokalemia. Rare cases of hypokalemia following high- and low-dose glucocorticoid injections have been reported. This study presents the history of a young, healthy male without significant past medical history who presented with an inability to stand and walk due to four-limb paralysis (more prominent in the lower limbs) following an intramuscular injection of a 4 mg betamethasone, which was prescribed for the treatment of allergic rhinitis. The patient was stabilized with an intravascular injection of potassium chloride diluted in 1000 mL of normal saline and monitored for 24 h, ruling out any other endocrine condition. Hypokalemia and its severe form are defined as the serum level of lower than 3.5 and 2.5 mEq/Lit, respectively. One of the etiologies of drug-induced hypokalemic paralysis is systemic glucocorticoid administration. In severe cases, it can cause quadriplegia and other neuromuscular, respiratory, and cardiac complications. Therefore, it is an urgent condition that should be managed carefully. Pregnant women who are receiving these medications are a specific group at risk of hypokalemic paralysis. There are several safer treatments for seasonal allergic rhinitis compared to systemic glucocorticoids, which should be considered by physicians. Moreover, paralysis in patients receiving these medications should be approached attentively since it might be caused by hypokalemia, which can be life threatening if not treated. It is advisable that the blood level of electrolytes, especially potassium, be checked for patients who present with paralysis or weakness after glucocorticoid injections.

Unveiling the Uncommon: Cushing's Syndrome (CS) Masquerading as Severe Hypokalemia.

Cushing's syndrome (CS) arises from an excess of endogenous or exogenous cortisol, with Cushing's disease specifically implicating a pituitary adenoma and exaggerated adrenocorticotropic hormone (ACTH) production. Typically, Cushing's disease presents with characteristic symptoms such as weight gain, central obesity, moon face, and buffalo hump. This case report presents an unusual manifestation of CS in a 48-year-old male with a history of hypertension, where severe hypokalemia was the primary presentation. Initial complaints included bilateral leg swelling, muscle weakness, occasional shortness of breath, and a general feeling of not feeling well. Subsequent investigations revealed hypokalemia, metabolic alkalosis, and an abnormal response to dexamethasone suppression, raising concerns about hypercortisolism. Further tests, including 24-hour urinary free cortisol and ACTH testing, confirmed significant elevations. Brain magnetic resonance imaging (MRI) identified a pituitary macroadenoma, necessitating neurosurgical intervention. This case underscores the rarity of CS presenting with severe hypokalemia, highlighting the diagnostic challenges and the crucial role of a collaborative approach in managing such intricate cases.

Cryptosporidium-induced acute kidney injury in a patient with acquired immunodeficiency syndrome.

Cryptosporidium is a pathogen that can cause infectious enteritis especially in immunocompromised patients. Acute kidney injury, electrolyte imbalance, and acid-base disorders may occur as a result of high volumes of intestinal fluid loss, which has not been previously reported to be a common manifestation of cryptosporidiosis. Numerous antigen detection methods can be used to ensure early diagnosis of Cryptosporidium infection, which is crucial to prevent morbidities. We report a unique case of cryptosporidiosis in a 33-year-old male patient with acute kidney injury and profound hypokalemia, hyponatremia, hypocalcemia, hypophosphatemia, hypomagnesemia, and metabolic acidosis. Following the initiation of antiretroviral therapy to human immunodeficiency virus, the patient's symptoms improved and he recovered fully from kidney injury and electrolyte imbalance, highlighting the importance of early antiretroviral therapy.

Simultaneous Occurrence of Hyponatremia and Hypokalemia in a Patient with Herpes Zoster: A Case Report with a Review of the Literature.

We herein report a patient with herpes zoster (HZ), severe hyponatremia, and hypokalemia. Syndrome of inappropriate antidiuresis (SIAD) leads to euvolemic hyponatremia and hypoosmotic plasma due to inadequate diuresis. Hyponatremia in the current patient was caused by SIAD and associated with HZ of the trigeminal facial nerve (V1). The patient also had hypokalemia, with excessive urinary potassium excretion and elevated cortisol levels. Hypokalemia is caused by hypercortisolemia, which is stimulated by HZ pain. Adequate treatment for HZ and comprehensive pain control play pivotal roles in improving SIAD, cortisol hypersecretion, and the subsequent electrolyte abnormalities.

Abiraterone-Induced Secondary Hypertension: Two Wrongs Don't Make a Right.

Abiraterone, an inhibitor of both 17α-hydroxylase and 17,20-lyase, is considered a novel, state-of-the-art, life-prolonging therapy in the urologists' arsenal when treating prostate cancer. Despite its efficacy, it is linked with an increased risk of cardiovascular adverse effects. Herein, we report a case in which the administration of abiraterone resulted in a full-blown syndrome of apparent mineralocorticoid excess despite the concomitant administration of prednisolone; that is, secondary hypertension, hypokalemia, metabolic alkalosis, as well as elevated levels of adrenocorticotropic hormone (ACTH).