Colistin-induced Bartter-like Syndrome: Ponder before Treatment!

Bartter-like syndrome (BLS) is a constellation of biochemical abnormalities which include metabolic alkalosis, hypokalemia, hypocalcemia, hypomagnesemia with normal kidney function. BLS is a very rare syndrome and can be induced by certain diseases, antibiotics, diuretics, and antineoplastic drugs. Colistin is a polymicrobial bactericidal drug and currently re-emerged as the only salvation therapy against multidrug resistant bacilli especially in critically ill patients at intensive care units. Only an anecdotal case report of colistin-induced Bartter-like syndrome has been reported. We here report a case series of four critically ill patients who were on treatment with colistin and presented with serious metabolic disturbances. How to cite this article: Kumari A, Gupta P, Verma H, Kumar A, Thakur P, Sharma K. Colistin-induced Bartter-like Syndrome: Ponder before Treatment! Indian J Crit Care Med 2022;26(2):239-243.

Acquired Bartter-like Syndrome Presenting with Polyuria and Reversible Hypokalemia Associated with Colistin Use in a Critically Ill Pediatric Patient.

We report a case of an acquired Bartter-like syndrome (BLS) after 3 days of treatment initiation and improved after discontinuation of colistin therapy in pediatric intensive care unit. A 2-month-old girl with spinal muscular atrophy type 1 who had respiratory distress received colistin therapy with a dose of 5 mg/kg/day for Acinetobacter baumannii complex isolation from endotracheal aspirate on the 12th day follow-up. Polyuria (6 mL/kg/hour) in the presence of normal blood pressure and hypokalemic metabolic alkalosis were developed on the 3rd day of colistin treatment. Colistin was stopped on the 4th day, and 2 days after discontinuation of colistin, polyuria improved dramatically. Her metabolic alkalosis and hypokalemia discontinued after 2 and 4 days, respectively. There are very few reports about colistin-induced BLS. The onset of polyuria, hypokalemia, and metabolic alkalosis during treatment with colistin and resolution after interruption suggest a causative relationship. How to cite this article: Yavas DP, Ekinci F, Horoz OO, Gundeslioglu OO, Atmis B, Yildizdas D. Acquired Bartter-like Syndrome Presenting with Polyuria and Reversible Hypokalemia Associated with Colistin Use in a Critically Ill Pediatric Patient. Indian J Crit Care Med 2021;25(7):822-824.

Acquired Bartter-like syndrome associated with colistin use in an adult patient: a case report.

Colistin is an effective antibiotic utilized for the treatment of Gram-negative bacterial infections with coverage against a broad spectrum of bacteria. Despite the broad antibacterial coverage, this antibiotic can have serious complications such as acute kidney injury. Colistin also can have a toxic effect on the loop of Henle, causing tubulopathy, electrolyte imbalances, and the occurrence of Bartter-like syndrome (BLS) which is characterized by magnesium and calcium disturbances, polyuria, and metabolic alkalosis. We here report a 32-year-old male with a history of multiple trauma due to an accident that received colistin therapy for Pseudomonas isolation from wound culture on the 5th day of hospitalization. Polyuria, hypokalemic metabolic alkalosis, hypomagnesemia, and hypocalcemia were developed on the first week of colistin administration. The patient received colistin until the 21st day of hospitalization. Serum calcium and magnesium levels became normal 1 day after stopping colistin, while urine volume and metabolic alkalosis resolved 6 days after colistin discontinuing. Therefore, it is crucial to adjust the dose of colistin to minimize its toxicity.

Bartter-like Syndrome Induced By Tacrolimus in a Renal Transplanted Boy: A Case Report.

BACKGROUND: Losing-salt tubulopathies, such as Bartter syndrome, are rare and usually inherited due to mutations of tubular reabsorption channels of the nephrons. Despite its scarcity, some cases of acquired losing-salt tubulopathies have been described. In this case report, we discuss the main aspects of Bartter syndrome and present a rare pediatric case of probable tacrolimusinduced Bartter-like syndrome in a renal transplanted boy. CASE PRESENTATION: A ten-year-old male patient with end-stage renal disease due to endo and extra capillary glomerulonephritis was submitted to renal transplantation from a deceased donor. The post-operatory evolution was satisfactory with normalization of serum creatinine levels, mild hypertension, and the absence of metabolic disorders. The immunosuppression protocol included tacrolimus (0.3 mg/kg/day), mycophenolate (455 mg/m2/day) and prednisone (0.5 mg/kg/day). Two months later, the patient was hospitalized due to vomiting, dehydration, intense hypokalemia (1.3 mEq/L), hyponatremia (125 mEq/L), and hypochloremia (84 mmol/L). During hospitalization, he evolved with polydipsia (3000 mL/day) and polyuria (120-160 mL/m2/h) associated with major elevation of urinary potassium excretion, hypercalciuria, mild metabolic alkalosis, hyperfiltration, and proteinuria. The tacrolimus dose was reduced under the suspicion of tubular dysfunction, leading to a better metabolic profile. However, the patient developed a Banff IIb graft rejection, which required pulse therapy and elevation of tacrolimus and mycophenolate doses. Recovery of renal function parameters occurred, but the metabolic disorders worsened following tacrolimus dose elevation. The patient required chronic potassium, chloride, and sodium replacement. CONCLUSION: After administering immunosuppressive medications, physicians should be aware of the possibility of Bartter-like or other losing-salt tubulopathies syndromes that can affect metabolic homeostasis. The suspicion must always be considered in the case of a transplanted patient who presents dehydration and hydroelectrolytic disorders right after the commencement of nephrotoxic immunosuppressive drugs, including tacrolimus and cyclosporine.

IV Colistin: A Rare Cause of Bartter-Like Syndrome in Adults.

Bartter syndrome is a genetic condition characterized by autosomal recessive inheritance, resulting in impaired salt reabsorption and clinical manifestations such as low/normal blood pressure and extracellular fluid volume depletion. Multiple abnormalities of the electrolytes, including decreased potassium as well as chloride levels and, in some instances, hypomagnesemia, are its defining features. Metabolic alkalosis, hypokalaemia, hypocalcemia, and hypomagnesemia, together with adequate renal function, are all components of the Bartter-like syndrome. It is associated with certain antibiotics and antineoplastic drugs. We report a case of traumatic brain injury with pneumothorax who was on treatment on colistin and presented with metabolic disturbance.

Bartter-Like Syndrome as the Initial Presentation of Dent Disease 1: A Case Report.

Dent disease is a rare genetic disease characterized by low-molecular-weight proteinuria. Dent disease with Bartter-like syndrome is rare and can easily be misdiagnosed and mistreated. Herein, we report a case of Dent disease 1 with Bartter-like syndrome as the initial manifestation. The patient was admitted to The Second Xiangya Hospital of Central South University due to polydipsia, polyuria, and weakness of both lower limbs at 2 years of age. Laboratory tests showed that serum sodium, potassium and chlorine levels were low, while serum creatinine levels were normal. The calcium level in the urine was normal. The patient was initially diagnosed with Bartter syndrome, and despite medical interventions, he eventually developed chronic kidney disease stage 4 at 13 years of age. To determine the cause, the patient was recommended to undergo genetic testing, which showed a CLCN5 gene c. 941C > T mutation (p.S314L), and was finally diagnosed as Dent disease 1. The clinical manifestations of Dent disease are complex and diverse. For patients with atypical clinical manifestations or unsatisfactory therapeutic effects, genetic testing is recommended.

[Secondary hyperaldosteronism and medullary nephrocalcinosis caused by self-administered and uncontrolled laxative use in an adolescent patient].

Secondary hyperaldosteronism is respondent aldosterone secretion increase, occurring due to some diseases or drug use. It may be accompanied by normal arterial pressure with/without water retention or arterial hypertension without water retention. Secondary hyperaldosteronism without arterial hypertension and without water retention is usually caused by the use of laxative and diuretic drugs. This condition is characterized by the lack of salt wasting symptoms, presence of myalgia and muscle weakness resulting from hypokalemia, calcium oxalate crystalluria and sonographic signs of medullary nephrocalcinosis. Such characteristics of water-salt exchange and presence of nephrocalcinosis in combination with hypercalciuria are defined as Bartter-like syndrome. Peculiarity of the given clinical case is determined not by a diagnostic difficulty of secondary hyperaldosteronism but concealment of long term self-administered use of laxatives 2 years without medical indications in a female patient, resulting in medullary nephrocalcinosis. A well-informed patient may endanger medical practice, because it is impossible to foresee everything including the uncontrolled self-administered drug use leading to the undesirable consequences.

Acquired Bartter syndrome following gentamicin therapy.

Aminoglycoside nephrotoxicity may manifest as nonoliguric renal failure or tubular dysfunction, such as Fanconi-like syndrome, Bartter-like syndrome (BS), or distal renal tubular acidosis. We report a case who developed severe renal tubular dysfunction on the the 7th day of gentamicin therapy, resulting in metabolic alkalosis, refractory hypokalemia, hypocalcemia, hypomagnesemia, and polyuria. The patient was diagnosed as a case of transient BS associated with gentamicin exposure. The patient recovered with conservative management.

A Case of Bartter-like Syndrome in a Patient of Drug-induced Interstitial Nephritis Associated with Rheumatoid Arthritis / 대한신장학회잡지

A 59-year-old female patient with rheumatoid arthritis showed hypokalemic metabolic alkalosis, normotensive hyperreninemic hyperaldosteronism and high urinary prostaglandin level. She was thought to have Bartter's syndrome. But, her kidney biopsy specimen showed chronic interstitial nephritis. She have used acetaminophen containing analgesics for recent three years. So we thought her disease was caused by drug. But, in this case, clinical manifestations are correspond with Bartter's syndrome and we have witnessed a successful respond to kalium replacement, angiotensin converting enzyme inhibitor, prostaglandin inhibitor and spironolactone administration.

Evaluation of Bartter-like Syndrome Associated with Aminoglycoside Micronomocin Sulfate Administration During Acute Pyelonephritis Treatment / 대한신장학회잡지

The aminoglycoside antibiotics is widely used in the treatment of infectious caused by gram-negative bacteria and for synergistic effect with(beta-lactam antibiotics. However, its therapeutic usefulness is limited by this potential nephrotoxicity and by disturbance of electrolyte homeostasis resulting in hypomagnesemia, hypokalemia, hypocalcemia such as Bartter-like syndrome. Many case repots have been reported on development of Bartter-like syndrome after aminoglycosides administration. But these reports had the many differences of such as types of aminoglycosides, age of patients, duration and total dose of treatment, combined antibiotics and baseline diseases. Therefore, the purpose of this study is to assess the effects of micronomocin sulfate on magnesium, calcium and potassium status of patients in acute pyelonephritis. Twenty one patients in acute pyelonephritis(18 female/3 male, ages 20-75) was treated with single or combined antibiotics. Eleven of twenty one patients as study group were treated with both micronomicin sulfate(aminoglycoside, 4mg/kg/day, during 5-8days) and flomoxef sodium (3rd cephalosporine, 2g/day, during 5-8days), and ten of twenty one patients as control group were treated only with flomoxef sodium(3rd cephalosporine. 2g/day. during 5-8days). Renal values, plasma and urinary electrolytes were measured before and at the end of IV antibiotic therapy. After micronomicin sulfate administrated for 6.4+/-1.5days, serum Mg, Ca, K, FEMg (fractional excretion of Mg), TTKG(transtubular K concentration gradient) and FECa(fractional excretion of Ca) did not significantly change(p>0.05). Therefore, those results suggest that micromonicin sulfate therapy within dose of 240mg/day(4mg/kg/day) for 6.4+/-1.5days may not cause disturbance of electrolyte homeostasis such as Bartter-like syndrome in acute pyelonephritis. Howerever, electrolyte disturbance is an important complication when aminoglycosides is given in larges doses over extended periods. Therefore, monitoring of blood concentration and urinary losses of electrolyte should be carried out along with careful observation of Bartter-like syndrome.