Piperacillin-tazobactam is a generally well-tolerated broad-spectrum antibacterial. Mild hypokalemia may occur with piperacillin-tazobactam therapy as a result of increased renal potassium losses. Severe hypokalemia is rare. We report here a case of very severe hypokalemia during piperacillin-tazobactam therapy, refractory to aggressive potassium replacement.
Background:Primary hyperoxaluria Type 1 is a rare inherited metabolic disorder caused by pathogenic variants in the AGXT gene. Because the disorder leads to excessive internal oxalate formation, progressive end-stage kidney disease (ESKD) may occur. While most affected individuals present during childhood, a subset is diagnosed only later in adult life, frequently after substantial renal deterioration. Delayed diagnosis increases the risk of recurrent oxalate nephropathy and graft dysfunction following kidney transplantation. Case Presentation:We report a 30-year-old woman with ESKD of unknown aetiology who underwent living-donor kidney transplantation. One year later, during a subsequent pregnancy, she developed progressive graft dysfunction. Kidney biopsy demonstrated extensive calcium oxalate crystal deposition, raising suspicion for an underlying metabolic disorder. Genetic testing subsequently confirmed a pathogenic AGXT mutation, establishing the diagnosis of adult-onset PH1. Urinary oxalate concentrations were within normal limits before and after transplantation, emphasizing the diagnostic challenge. Conclusion:This case highlights the importance of considering PH1 in adults with unexplained chronic or ESKD, even in the absence of classical features or elevated urinary oxalate excretion. Early genetic testing and careful assessment of family history are essential for timely diagnosis, enabling appropriate transplant planning, disease-specific therapy, and genetic counselling.
Background:Frequently relapsing nephrotic syndrome (FRNS) and steroid-dependent nephrotic syndrome (SDNS) are distinct phenotypes defined by relapse frequency and the temporal relationship of relapse to prednisolone therapy, respectively. Both remain therapeutic challenges despite the use of corticosteroid-sparing agents. Relapses may be triggered by intercurrent infections and can be complicated by significant edema, hypoalbuminemia, and infection risk, requiring prompt optimization of immunosuppressive and supportive therapy. Case Presentation:An 11-year-old boy with SDNS presented with a two-day history of bilateral periorbital swelling and facial puffiness following fever, rhinorrhea, and productive cough. He had experienced 11 previous relapses and was receiving ciclosporin 50 mg twice daily and enalapril 5 mg once daily with good adherence. Previous kidney biopsy showed minor glomerular change, and ciclosporin trough concentration was therapeutic. On admission, he was febrile (38.3°C) with leukocytosis, neutrophilia, thrombocytosis, marked hypoalbuminemia, significant proteinuria, and hematuria. Penicillin V was initiated for spontaneous bacterial peritonitis prophylaxis. Prednisolone was optimized from 40 mg once daily to 30 mg twice daily based on a body surface area of 1.17 m2. Progressive edema and weight gain required escalation to intravenous frusemide with 20% human albumin, resulting in marked clinical improvement. Proteinuria, hematuria, and ascites resolved, and he was discharged clinically stable with minimal residual edema. Conclusion:This case highlights several important therapeutic considerations in relapsing childhood nephrotic syndrome: recognition of SDNS as a subgroup of SSNS, accurate prednisolone dosing during relapse, careful assessment of edema and intravascular volume status before diuretic therapy, and individualized use of steroid-sparing agents and antimicrobial prophylaxis. In children receiving prolonged ciclosporin therapy, treatment should be regularly reviewed with blood pressure, renal function, and therapeutic drug monitoring in view of potential calcineurin inhibitor toxicity, and alternative steroid-sparing options such as levamisole may be considered where clinically appropriate.
Atheroembolic renal disease (AERD) is an underdiagnosed condition with diverse clinical presentations that can mimic various renal pathologies. Most cases follow intravascular procedures or anticoagulation, while only rare case reports of spontaneous AERD have been described. We present two contrasting cases of AERD with markedly different presentations. The first patient was a 74-year-old male who presented with worsening dyspnoea, acute renal failure and skin changes following coronary bypass surgery, typical of AERD. The second patient was a 70-year-old male who presented with symptomatic hypertension and acute-on-chronic kidney injury without identifiable precipitating factors, initially suspected to be rapidly progressive glomerulonephritis. Renal biopsies revealed cholesterol emboli within arteries, characterised by needle-shaped clefts surrounded by foreign body giant cells, with background interstitial fibrosis and tubular atrophy confirming the diagnosis. These contrasting cases demonstrate the diagnostic challenges of AERD and highlight the importance of renal biopsy for accurate diagnosis in both classic and atypical presentations.
Introduction:Thrombotic microangiopathies (TMAs) are a group of rare, life-threatening disorders characterized by a classic triad of MAHA, severe thrombocytopenia, and ischemic tissue injury. Thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) are the main types of TMAs. Based on the cause, HUS can be classified as typical or atypical. Case Presentation:We present the case of a 4-year-old child referred to King Fahad Medical City in Riyadh, Saudi Arabia, with complaints of bloody diarrhea, vomiting, and fever. The condition progressed to altered consciousness, seizures, and quadriparesis. Result:Upon admission, the patient received plasma infusion and underwent peritoneal dialysis. Eculizumab therapy was initiated 1 week after the presentation. Hematological and renal parameters improved rapidly, but neurological recovery was gradual, with significant progress observed over 6 years of follow-up. Conclusion:This case highlights that severe neurological manifestations can be an initial feature of HUS, not just TTP. Eculizumab was effective and life-saving in pediatric patients with TMA and severe neurological involvement, though CNS recovery may take years.
Background:Exercise-induced rhabdomyolysis results from skeletal muscle injury after strenuous or unaccustomed exertion. Acute kidney injury is a feared complication, but creatine kinase magnitude alone is an imperfect predictor of kidney injury. Case Presentation:A 24-year-old previously healthy male presented with dark urine after one week of high-intensity resistance and eccentric exercise as a novice participant in structured high-intensity training. He reported daily oral hydration of more than 2.5 L and denied creatine monohydrate use. Initial tests showed creatine kinase of 79,038 U/L, creatinine of 1.3 mg/dL, estimated glomerular filtration rate of approximately 79 mL/min/1.73 m2 by the 2021 CKD-EPI creatinine equation, aspartate aminotransferase (AST) of 507 U/L, and urine dipstick blood of 3+ with few red blood cells. Urea, potassium, calcium, magnesium, and phosphorus were within reference ranges, and urinalysis showed only trace protein without leukocytes or nitrites. He received isotonic intravenous fluids without bicarbonate, diuretics, or renal replacement therapy. Creatinine decreased to 0.6 mg/dL within 24 h and remained stable; urine dipstick blood became negative by Day 2; creatine kinase declined to 722 U/L by Day 10 and 287 U/L by Day 16, while creatinine remained normal at 0.7 mg/dL and aminotransferases improved to AST of 25 U/L and ALT of 42 U/L. Conclusion:This case is best interpreted as severe exertional rhabdomyolysis with pigmenturia and preserved renal function, rather than confirmed intrinsic acute kidney injury. The report highlights the need to avoid creatine kinase-centric risk assessment and to interpret a mildly elevated admission creatinine in context, especially when rapid normalization follows fluid resuscitation.
Aim Through the lens of a clinical case, we explore the overlap in pathophysiology between Alport syndrome and seronegative inflammatory arthritis, focusing on the collagen structural changes that can occur in Alport syndrome. Results Genetic variant information was obtained for a patient diagnosed with Alport syndrome. Few cases of Alport syndrome associated with inflammatory arthritis have been reported in the literature so far. The genes encoding collagen fibrils affected in Alport syndrome are also expressed in hyaline cartilage. The inflammatory response triggered by these misfolded, truncated, or missing proteins may contribute to inflammatory pathways present in arthritis through compromised collagen structures. Clinical Takeaway Evaluation of hematuria and concomitant inflammatory arthritis should include consideration of hereditary connective tissue disorders, such as Alport syndrome.
Introduction:Liddle's syndrome is a rare inherited disorder associated with early-onset and resistant hypertension due to hyperactivity of epithelial sodium channels (ENaCs). The condition is caused by mutations in the genes SCNN1A, SCNN1B, and SCNN1G. Liddle's syndrome leads to hypertension, hypokalemia, and metabolic alkalosis. Case Presentation:A previously healthy 21-year-old male patient complained of severe central chest pain radiating to both arms and had a hypertensive emergency with a BP reading of 267/170 mmHg. The patient had marked elevation in troponin I (13.9 ng/mL), hypokalemia (2.8 mmol/L), and metabolic alkalosis. The electrocardiogram showed left ventricular hypertrophy with a strain pattern and QTc prolongation due to hypokalemia. Coronary angiography ruled out the possibility of primary acute coronary syndrome by revealing normal coronary arteries. Echocardiogram showed concentric left ventricular hypertrophy with normal ejection fraction and no wall motion abnormalities. In search of the secondary cause of hypertension, renal Doppler ultrasonography and aldosterone-to-renin ratio were normal, thus ruling out primary hyperaldosteronism. About the typical clinical and biochemical presentation, a clinical diagnosis of Liddle syndrome was highly likely. Genetic tests were not performed owing to financial constraints. However, treatment with amiloride brought about remarkable improvement in the control of hypertension and normalization of potassium levels. Conclusion:Liddle's syndrome should be suspected in cases where there are young individuals who have severe hypertension, hypokalaemia, and an aldosterone-to-renin ratio that is normal or low. The diagnosis must be made promptly because delay may lead to complications. In instances where molecular testing is impractical, treatment with ENaC inhibition using amiloride is diagnostic and potentially life-saving.
Perinuclear antineutrophil cytoplasmic antibodies (P-ANCAs) and myeloperoxidase (MPO) antibodies are detected in 15%-25% of lupus nephritis patients, but systemic lupus erythematosus (SLE)/ANCA-associated vasculitis (AAV) overlap syndrome is rare, occurring in approximately 2% of cases. We present a 57-year-old woman with SLE and antiphospholipid syndrome (APS) on belimumab, hydroxychloroquine, and prednisone, who presented with acute ischemic stroke requiring thrombectomy and rapidly progressive renal failure (creatinine rising from 1.1 to 5.2 mg/dL) with nephrotic-range proteinuria (8.6 g/g). P-ANCA titer was > 1:640 with MPO positivity, while anti-dsDNA, C3, and C4 were normal. Kidney biopsy revealed crescentic glomerulonephritis with neutrophil-rich infiltrates and immune complex deposits on electron microscopy but without "full house" immunofluorescence, favoring SLE/AAV overlap rather than isolated lupus nephritis flare. Treatment with methylprednisolone, rituximab, and anticoagulation resulted in significant renal recovery (creatinine 1.7 mg/dL, proteinuria 4.4 g/g). This case highlights the importance of ANCA testing in SLE patients with unexplained rapidly progressive glomerulonephritis, as early recognition of overlap syndrome carries distinct therapeutic implications, including the use of rituximab-based regimens targeting both disease processes.
Diabetes insipidus (DI) is a heterogeneous disorder characterised by polyuria and polydipsia due to impaired arginine vasopressin (AVP) secretion or action. We describe a 36-year-old pregnant woman who presented at 28 weeks' gestation with weakness, severe hypokalaemia from renal potassium wasting, hypernatraemia and polyuria with dilute urine. Vasopressinase-mediated DI was suspected; there was no response to AVP, but desmopressin (dDAVP) produced a rapid clinical improvement, confirming the diagnosis. However, postpartum recurrence of symptoms prompted further evaluation, with imaging suggestive of lymphocytic infundibuloneurohypophysitis, necessitating reinitiation of dDAVP. This case highlights the diagnostic complexity of DI in pregnancy and the need to remain vigilant for central causes, even when vasopressinase-mediated DI is initially suspected.
We herein report the case of a 2-year-old girl with novel compound heterozygous NPHS1 variants, p.R460Q (a known loss-of-function mutation) and p.V822M (a rare variant with reported pathogenicity and relatively mild functional effects). She initially presented with typical features of idiopathic nephrotic syndrome and achieved complete remission on Day 10 of corticosteroid therapy. After tapering, the patient developed recurrent episodes of infection-associated heavy proteinuria, which often remitted spontaneously but sometimes left residual low-grade proteinuria. Despite the introduction of cyclosporine, these episodes continued, and the effect of immunosuppression remained unclear. Over a 4-year follow-up, recurrent transient proteinuria persisted, but no relapse of nephrotic syndrome or renal dysfunction was observed. This atypical clinical pattern, characterized by incomplete remissions and limited response to immunosuppressive therapy, prompted genetic testing, which revealed compound heterozygous NPHS1 variants. This case expands the phenotypic spectrum of NPHS1-associated disease, thus highlighting that nephrin variants may manifest as steroid responsiveness, preserved renal function, and repeated transient proteinuria. Our findings emphasize the role of genetic testing in clarifying diagnosis and guiding management in steroid-sensitive nephrotic syndrome with atypical features.
Background:Takayasu arteritis (TAK) is a chronic granulomatous large-vessel vasculitis that predominantly affects the aorta and its major branches, leading to stenosis, occlusion, or aneurysmal changes. Renal artery disease is common, but acute bilateral renal artery thrombosis causing renal dysfunction is rare. Case presentation:A 38-year-old South Asian male presented with a two-week history of abrupt-onset bilateral loin pain and severe azotemia (creatinine 8.25 mg/dL). Inflammatory markers were high (ESR 102 mm/h; CRP 45 mg/L). Ultrasound showed preserved renal size; Doppler suggested globally poor bilateral renal perfusion. CT angiography revealed bilateral renal artery thrombosis, mural thickening of the renal arteries, and a distal abdominal aortic dissection extending to the iliac arteries. Infectious, autoimmune, and limited thrombophilia screens were negative. The clinical and radiological constellation was most consistent with TAK, based on imaging evidence of large-vessel vasculitis involving bilateral renal arteries and compatible clinical findings. A multidisciplinary team (nephrology, vascular surgery, and rheumatology) advised anticoagulation due to bilateral renal artery thrombosis despite the distal Type B dissection. He received intravenous methylprednisolone followed by oral prednisolone, with recovery of renal function to 1.8 mg/dL and normalization of inflammatory markers in a month. Conclusions:In young adults presenting with abrupt bilateral renal ischemia and systemic inflammation, TAK should be considered. Early vascular imaging and prompt immunosuppression can preserve renal function. Anticoagulation therapy may be justified in selected cases of thrombosis even in the presence of limited dissection, provided decisions are multidisciplinary and blood pressure is tightly controlled.
Gitelman syndrome (GS) is a rare inherited renal salt-wasting tubulopathy characterized by hypokalemia, hypomagnesemia, and hypocalciuria. Its nonspecific presentation often overlaps with that of more common pediatric conditions, leading to delayed diagnosis, particularly in resource-limited settings. We report an 11-year-old boy who presented with progressive weight loss, polyuria, polydipsia, and salt craving. His course was complicated by recurrent episodes of severe hypokalemia and hypomagnesemia, and he was initially evaluated for diabetes mellitus, other endocrine disorders, chronic infections such as tuberculosis, and malnutrition without a definitive diagnosis. During the index admission, he developed acute worsening of muscle weakness associated with severe hypokalemia and hypomagnesemia and biochemical findings consistent with renal salt wasting, supporting a diagnosis of GS in the absence of genetic testing. Management with correction of hypovolemia, electrolyte supplementation, liberal salt intake, and nutritional support led to marked clinical improvement and stabilization of biochemical abnormalities on follow-up. This case highlights the importance of maintaining a high index of suspicion for GS in children presenting with polyuria, polydipsia, salt craving, and unexplained electrolyte disturbances, particularly in resource-limited settings.
Introduction:Mercuric chloride is a highly toxic inorganic compound with historical medical use but severe potential for harm when ingested. Acute mercury poisoning is rare but can lead to multiorgan toxicity, particularly affecting the kidneys and gastrointestinal tract. Prompt recognition and intervention are essential to prevent long-term sequelae and mortality. Case Presentation:An 18-year-old male with a psychiatric history presented one hour after intentional ingestion of five mercuric chloride tablets. He exhibited mild abdominal symptoms, and initial laboratory studies revealed proteinuria, glycosuria, and rising creatinine. Imaging showed echogenic kidneys, and serum mercury levels were markedly elevated at 840 μg/L. He was treated with oral dimercaptosuccinic acid (DMSA), intravenous fluids, and gastrointestinal decontamination. Despite therapy, his renal function declined, with creatinine peaking at 9.6 mg/dL, requiring hemodialysis. Renal biopsy demonstrated acute tubular necrosis without immune complex deposition. After six sessions of hemodialysis and 16 days of chelation therapy, renal function and mercury levels improved, allowing discharge to psychiatric care. Discussion:Mercuric chloride exerts its nephrotoxic effects primarily through oxidative injury to proximal tubular cells, resulting in acute tubular necrosis. While chronic mercury exposure is more often associated with glomerular diseases, acute ingestion more typically causes tubular injury. Chelation with DMSA facilitates mercury elimination but may be insufficient when renal impairment occurs. In such cases, hemodialysis becomes essential for toxin clearance and metabolic support. This case underscores the importance of early, combined therapeutic interventions. Conclusion:Acute mercuric chloride ingestion is a medical emergency that can cause life-threatening renal toxicity. Timely initiation of chelation therapy and supportive measures, including hemodialysis, are crucial for recovery. This case demonstrates that even in severe presentations, multidisciplinary management can result in favorable outcomes.
IgA nephropathy (IgAN), or Berger's disease, is the most common primary glomerulopathy worldwide. It is characterized by dominant mesangial deposition of immunoglobulin A1 (IgA1), typically of the galactose-deficient form (Gd-IgA1), which triggers the formation of circulating immune complexes and subsequent glomerular inflammation. Clinical presentation includes hematuria, proteinuria, and, in severe cases, progressive renal failure. A rare variant is the extracapillary or crescentic form, which follows an aggressive course. We report the case of a 52-year-old woman with a history of Stage II right-sided infiltrating ductal breast carcinoma, treated in 2023 with radical mastectomy, AC-T chemotherapy, and radiotherapy. Complete oncologic remission was confirmed by SPECT imaging. In January 2025, with a known baseline creatinine of 1.2 mg/dL, the patient presented with macroscopic hematuria, hypertension, and rapid decline in renal function. Workup revealed subnephrotic proteinuria (1854 mg/24 h), active urinary sediment with 65% dysmorphic erythrocytes and red blood cell casts, and a creatinine peak of 4.7 mg/dL. Autoimmune serologies were negative. Kidney biopsy showed IgAN with cellular crescents in 64% of glomeruli and an Oxford classification of M0 E0 S1T1 C2. Immunofluorescence confirmed mesangial IgA and C3 deposits. Despite treatment with intravenous methylprednisolone, cyclophosphamide, and oral prednisone, yet no renal recovery was achieved, and the patient remains on chronic hemodialysis. To our knowledge, this is the first reported case in Bolivia of extracapillary IgAN occurring after breast cancer remission, highlighting a rare clinical association and raising the possibility of an underlying immune-mediated link between malignancy and crescentic IgAN, without establishing causality.
Background:Chronic kidney disease (CKD) is a major global health concern, with a substantial proportion of cases that remain of undetermined cause. Mutations in genes affecting podocyte structure and function, are increasingly recognized as causes of focal segmental glomerulosclerosis (FSGS), a common but highly nonspecific histological pattern of kidney injury, that ultimately lead to CKD. Case Presentation:We report the case of a 55-year-old male who presented with hypertension and end-stage renal disease (ESRD) of unknown etiology. He had a progressive decline in kidney function and proteinuria beginning in young adulthood. A kidney biopsy showed a pattern of FSGS. A comprehensive workup did not identify autoimmune or inflammatory causes. Whole-exome sequencing detected a previously undescribed heterozygous CRB2 mutation (c.1037G > T, p.Cys346Phe), predicted to be deleterious. Discussion:Animal models of CRB2 deprivation in podocytes showed progression toward FSGS. In humans, CRB2 mutations have previously been linked to severe early-onset nephrotic syndrome, typically in homozygous or compound heterozygous states. This is the first report of an adult-onset CRB2-associated FSGS in a heterozygous state, suggesting a milder disease course with a progressive kidney decline. As with other genetic forms of FSGS, we hypothesize that heterozygous CRB2 mutations may permit near-normal renal function for years until cumulative stressors trigger podocyte injury and CKD progression. Conclusion:This case expands the clinical spectrum of CRB2-related kidney disease and highlights the importance of genetic testing in adults with unexplained CKD. Identifying genetic forms of CKD may refine diagnostic and therapeutic approaches in nephrology.
Introduction:Disaster-related deaths (DRDs) are indirect fatalities caused by physical or psychological stress during evacuation. Patients undergoing hemodialysis (HD) face increased vulnerability during disasters due to reduced dialysis frequency, elevated mental stress, and limited access to medical resources. Although their risk is heightened, detailed analyses of DRDs in HD patients remain sparse. Methods:This retrospective study analyzed 13 HD-related DRD cases in Minamisoma City, Fukushima Prefecture, following the Fukushima Daiichi Nuclear Power Plant accident. A total of 520 DRDs were certified in the city. Data from local government records were extracted, focusing on time of death, causes of death, and psychiatric symptoms. Results:The mean age (± standard deviation) at death for HD patients was 77.92 (±8.37) years, which was younger than the mean age (± standard deviation) of 82.81 (±11.97) years among non-HD individuals (Welch's t-test, p = 0.060). Most deaths occurred during the chronic phase of the disaster. Primary causes included exacerbation of chronic kidney disease, cardiovascular complications, and sepsis. Over half of the patients exhibited psychiatric symptoms such as depression or mood instability. Discussion:This case series illustrates the severe impact of disruptions in medical care and the stress of repeated evacuations. Challenges include insufficient continuity of care and prolonged psychological distress, particularly during the chronic disaster phase. Our findings suggest that ensuring uninterrupted HD and providing long-term psychological support may be essential to mitigating DRDs in this population.
This is the first detailed report of spontaneous remission of late relapsing membranous nephropathy (MN) after previous immunosuppressant-induced remission. In March 2004, a 52-year-old Hispanic male presented with severe nephrotic syndrome with proteinuria of 13 g/24 h. The workup for infectious and autoimmune diseases was unrevealing. Renal biopsy showed MN (Stage II). A CT scan showed no malignancy but left pulmonary embolism and left renal vein thrombosis. Anticoagulation was started for asymptomatic thromboembolism. He achieved sustained complete remission of nephrotic syndrome after a prolonged, complicated treatment course of multiple immunosuppressants (corticosteroids and mycophenolate mofetil for 1 year, followed by alternating monthly corticosteroids and chlorambucil for 6 months, and again corticosteroids and mycophenolate mofetil for 6 years). Then in July 2021 (now at the age of 69 years), he developed nephrotic syndrome again with proteinuria of 6 g/24 h. Serological work-up was all negative except for the elevated serum Antiphospholipase A2 receptor (PLA2R) antibody at 42 RU/mL (nl < 14). Renal biopsy in November 2021 showed again MN (Stage III to IV). Immunohistochemistry staining of the biopsy tissue for PLA2R1 antigen was positive. A decision was made to observe him instead of starting immunosuppressants. He was treated with diuretics and Lisinopril. Anti-PLA2R antibody steadily improved to normal range and the nephrotic syndrome gradually improved and finally resolved by August 2023. There was no recurrence of nephrotic syndrome up to the most recent visit in March 2026. A review of the literature shows that a repeat biopsy in patients already known to have MN (especially those PLA2R-mediated cases) with relapse of nephrosis and stable renal function may not be necessary. In routine practice, the watchful waiting strategy for relapse of MN is less often taken as it should be. Therefore, more patients with relapsing MN deserve an observation period before starting immunosuppressants. Hopefully, KDIGO guidelines can include this point for relapsing MN.
Bowel perforation is a rare but serious complication of Tenckhoff catheter placement for peritoneal dialysis (PD), particularly when blind insertion techniques such as the Seldinger method are used. Standard management typically involves catheter removal, surgical repair of the bowel, and delayed reinsertion of a new catheter following completion of systemic antibiotic therapy. Although this approach minimizes the risk of infection, it necessitates a second surgical procedure and can significantly delay the initiation of PD. We report the case of a 60-year-old woman with end-stage kidney disease secondary to diabetic nephropathy who developed small bowel perforation during Tenckhoff catheter insertion via the Seldinger technique. To avoid a second operation, and in accordance with the patient's preference, simultaneous catheter removal and contralateral reinsertion were performed during surgical repair of the perforation. The peritoneal cavity was irrigated with 2.5 L of normal saline, a drain was placed, and the patient received a 14-day course of intravenous meropenem with peritoneal rest. The drain was removed on postoperative Day 5, and automated PD was successfully resumed two weeks later without any evidence of peritonitis. This case suggests that simultaneous catheter removal and reinsertion during bowel repair may be technically feasible under specific, favorable intraoperative conditions, potentially avoiding an additional procedure and facilitating earlier return to PD. However, this approach is not supported by current guidelines, which recommend delayed catheter reinsertion to allow adequate peritoneal healing, and should not be considered standard practice.
Background:Baclofen is a centrally acting muscle relaxant used orally and intrathecally for the management of spasticity, muscular spasms, and refractory hiccups. Baclofen is predominantly absorbed via the gastrointestinal tract, with over 80% excreted via the kidneys; hence, individuals with end-stage renal disease (ESRD) are at a heightened risk for baclofen toxicity. Baclofen can penetrate the blood-brain barrier, resulting in neurotoxicity. The potential of baclofen to induce acute pancreatitis is inadequately comprehended, with a limited number of instances documented in the medical literature. This report details an uncommon instance of an ESRD patient undergoing hemodialysis who had both baclofen-induced neurotoxicity and pancreatitis. Case Presentation:We present a case of a 55-year-old woman who is known to have ESRD; she is currently on hemodialysis three times a week. After only two baclofen doses (10 mg, 12 h apart), given for chronic cervical pain, the patient developed a profound decrease in her level of consciousness (LOC). The next day, when her LOC had improved after dialysis, she reported nausea, vomiting, and epigastric abdominal pain as well. Her initial laboratory report showed an elevated amylase level. So, the assessment was a baclofen neurotoxicity in an ESRD patient, which was accompanied by mild-moderate pancreatitis after only two doses. Since baclofen is highly dialyzable, she was commenced on daily conventional hemodialysis using a high-flux dialyzer for three consecutive days. She did not require continuous dialysis. Her LOC improved dramatically after the second session, and she returned to her baseline just after the third session. However, she reported headache and hallucinations after. Pancreatitis symptoms improved with supportive measures later. Conclusion:The case highlights the need for increased awareness among healthcare providers about the potential risks of baclofen use, particularly in patients with ESRD. Even a small dosing can cause neurotoxicity. This is a very rare case of baclofen neurotoxicity accompanied by pancreatitis, who did respond very well to conventional hemodialysis. Patients with decreased renal function should avoid using baclofen, as its accumulation depends on renal excretion capacity.
