0
selected
-
1.
Rhabdomyolysis and acute kidney injury induced by the association of rosuvastatin and abiraterone: A case report and review of the literature.
Ould-Nana, I, Cillis, M, Gizzi, M, Gillion, V, Hantson, P, Gérard, L
Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners. 2021;(1):216-219
Abstract
INTRODUCTION Abiraterone acetate is an inhibitor of androgens biosynthesis, approved as first-line treatment in castration-resistant prostate cancer and metastatic castration-sensitive prostate cancer. Abiraterone has been rarely associated with severe rhabdomyolysis, but the mechanism of muscle toxicity is unknown. CASE REPORT We hereby present a case of severe rhabdomyolysis resulting in acute on chronic kidney injury following abiraterone initiation in a patient previously under rosuvastatin. MANAGEMENT AND OUTCOME Rhabdomyolysis was resolutive after rosuvastatin and abiraterone discontinuation, and kidney function recovered. There was no recurrence of muscle toxicity after re-initiation of abiraterone alone. DISCUSSION Abiraterone selectively inhibits CYP17 as well as the hepatic transporter OATP1B1. OATP1B1 is an efflux transporter, whose function is to extract several drugs from the portal blood, allowing them to undergo hepatic metabolism. We hypothesize that abiraterone-induced inhibition of plasmatic uptake of rosuvastatin by OATP1B1 increased plasmatic concentration of rosuvastatin, leading to toxicity on muscle cells. We therefore suggest that the association between rosuvastatin and abiraterone should be avoided.
-
2.
Rhabdomyolysis associated acute renal failure - Report of two fatal cases and a brief review of literature.
Das, S, Hanuman, SB, Mylapalli, JL
Journal of forensic and legal medicine. 2020;:101941
Abstract
BACKGROUND Rhabdomyolysis is a potentially fatal condition which occurs due to skeletal muscle injury and classically presents with myalgia and red-brown coloured urine. Presence of excess myoglobin in the glomerular filtrate forms myoglobin casts which causes severe obstruction and necrosis of the tubules leading to acute renal failure. METHODS We report two fatal cases of rhabdomyolysis associated acute renal failure. The first victim died in police custody and the second victim died due to severe physical exertion. RESULTS In both the cases, creatine kinase levels were elevated and myoglobin was detected in urine in the second case. Myoglobin immunohistochemistry detected the presence of myoglobin cast in the glomerular tubules of kidney in both the cases. CONCLUSIONS Myoglobin immunohistochemistry of renal tissues, serum creatine kinase, urine myoglobin analysis and muscle histopathology are the laboratory tests that should be considered at autopsy where rhabdomyolysis is suspected.
-
3.
Osmolar-gap in the setting of metformin-associated lactic acidosis: Case report and a literature review highlighting an apparently unusual association.
Elshafei, MN, Alamin, M, Mohamed, MFH
Medicine. 2020;(41):e22492
-
-
Free full text
-
Abstract
RATIONALE Metformin-associated lactic acidosis (MALA) is a rare adverse effect that has significant morbidity and mortality. MALA is a high anion gap (AG), nonosmolar acidosis. Associated osmolar-gap (OG) is rarely reported, so finding an OG may make the diagnosis of MALA challenging. PATIENT CONCERNS Forty-five years' old type II diabetic patient on metformin presented to emergency with a two-day history of vomiting, watery diarrhea, and mild abdominal discomfort. On examinations, he looked dehydrated. Investigation revealed acute kidney injury (AKI) with a high lactic acid (LA) level of 24 mmol/L, pH of 6.8, AG of 40, and an OG of 20 mOsm/kg DIAGNOSES The presence of an OG made the diagnosis challenging; the history was negative for alcohol, osmolar substance, or illicit drug ingestion or use. The toxicology screen was negative. After ruling out plausible causes of AG and OG, MALA was deemed the likely reason for his presentation likely precipitated by dehydration and AKI. INTERVENTIONS He underwent two sessions of hemodialysis, afterward managed with fluid hydration. OUTCOMES On day 3, he was in the polyuric phase suggestive of acute tubular necrosis. His serum creatinine improved afterward with improved acidosis; after 8 days, he was discharged in stable condition. LESSONS MALA is a rare side effect of metformin therapy. Acute kidney injury is a known precipitant of MALA. In our review, we highlight the association of MALA and the presence of an OG. We believe that treating physicians should be aware of this relationship to avoid delaying or overlooking such an important diagnosis.
-
4.
Preventing kidney injury by avoiding fluid overload in patients with sepsis.
Dodd, RL, Archambault, ME
JAAPA : official journal of the American Academy of Physician Assistants. 2019;(12):40-45
Abstract
The global epidemiologic burden of sepsis is difficult to ascertain. Sepsis affects more than 31.5 million people worldwide every year, potentially resulting in 5 million deaths. Up to one-third of patients with sepsis also develop sepsis-associated acute kidney injury. This article describes the need for restraint in fluid resuscitation in patients with sepsis, in order to mitigate end-organ damage and ultimately to save lives.
-
5.
Generalized Status Epilepticus in a Patient with Acute-onset Type 1 Diabetes Mellitus Associated with Severe Kidney Dysfunction: A Case Report and Literature Review.
Ohara, N, Koda, R, Watanabe, H, Iino, N, Ohashi, K, Terajima, K, Ozawa, T, Ikeda, Y, Sekiguchi, H, Ohashi, H, et al
Internal medicine (Tokyo, Japan). 2017;(15):1993-1999
Abstract
A 65-year-old Japanese man with advanced chronic kidney disease (CKD) developed acute-onset type 1 diabetes mellitus (T1D) that was associated with severe acute kidney injury and was manifested by generalized tonic-clonic status epilepticus. His seizures resolved without recurrence after correcting the diabetic ketoacidosis. Although hyperglycemia is an important cause of acute symptomatic seizure (ASS), patients with ketotic hyperglycemia develop ASS less frequently. In this T1D case with CKD, severe hyperglycemia in conjunction with other metabolic insults, such as uremia, hyponatremia, and hypocalcemia, probably provoked his seizure despite the severe ketonemia.
-
6.
[Acute Kidney Injury in a Patient with Diarrhea and Vomiting Undergoing Chemotherapy for Colorectal Cancer].
Iwazu, Y, Kotani, K, Yamada, T
Rinsho byori. The Japanese journal of clinical pathology. 2016;(5):595-600
Abstract
A case of acute kidney injury (AKI) strongly suspected to be drug-induced (oxaliplatin and non-steroidal anti-inflammatory drug) is discussed regarding the mechanism of a reduced glomerular filtration rate responsible for the development of AKI. Urinary biochemical tests are useful for the differential diagnosis of pre- renal (functional) AKI and intrinsic (structural) AKI(so-called acute tubular necrosis). In this case, although a comprehensive differential diagnosis using these parameters supported intrinsic AKI, only one pa- rameter, fractional excretion of urea (FEurea), indicated the existence of prerenal AKI. As a result of treatment with the appropriate management of body fluid in addition to avoiding nephrotoxic medications, AKI rapidly improved. FEurea revealed the underlying mechanism of AKI. [Review].
-
7.
Neurological manifestation of recreational fatal and near-fatal diethylene glycol poisonings: case series and review of literature.
Imam, YZB, Kamran, S, Karim, H, Elalamy, O, Sokrab, T, Osman, Y, Deleu, D
Medicine. 2014;(10):e62
-
-
Free full text
-
Abstract
Diethylene glycol is a common industrial solvent which is responsible for accidental and epidemic poisoning as early as the 1930s. Due to the unavailability and unaffordability of ethanol, people in Qatar among the low income group are consuming household chemicals, some of which contain diethylene glycol, for recreational purposes.The history of ingestion is usually not volunteered and the initial clinical presentation is usually nonspecific, making it difficult to diagnose from the clinical presentation. Moreover, the biochemical profile varies with time, making the diagnosis more difficult. The neurological course and toxicity is less well characterized than its renal counterpart. Moreover, reports in the literature of such recreational poisoning is lacking particularly in the region.Three cases of recreational diethylene glycol poisoning seen in Hamad General Hospital, Doha, Qatar from 2009 to 2012 are detailed here.These illustrate the clinical course with emphasis on the neurological sequelae that include encephalopathy and multiple cranial and peripheral neuropathies with fatal and near-fatal outcomes. Neuroimaging in 2 were initially normal, but follow-up imaging showed brain atrophy. The third patient's neuroimaging showed diffuse brain edema with evidence of transtentorial herniation. Nerve conduction studies were performed in 2 of the 3 cases and showed evidence of mixed sensorimotor neuropathy. The outcomes were death in 1 and severe neurological morbidity and disability in 2 cases.Diethylene glycol is a dangerous substance when ingested and can result in mortality and severe morbidity, particularly from the renal and neurological manifestations. Whereas the mechanism of damage is less well known, the damage is likely dose related. The typical clinical pattern of evolution of the poisoning in the absence of cost-effective ways to detect it in the serum can help clinicians in making the diagnosis.Neurological manifestations may include encephalopathy and multiple cranial and peripheral neuropathies with subsequent brain atrophy. Public awareness of the danger of such recreational use should be raised.
-
8.
Acute kidney injury during therapy with an antisense oligonucleotide directed against PCSK9.
van Poelgeest, EP, Swart, RM, Betjes, MG, Moerland, M, Weening, JJ, Tessier, Y, Hodges, MR, Levin, AA, Burggraaf, J
American journal of kidney diseases : the official journal of the National Kidney Foundation. 2013;(4):796-800
Abstract
Antisense oligonucleotides have been explored widely in clinical trials and generally are considered to be nontoxic for the kidney, even at high concentrations. We report a case of toxic acute tubular injury in a healthy 56-year-old female volunteer after a pharmacologically active dose of a locked nucleic acid antisense oligonucleotide was administered. The patient received 3 weekly subcutaneous doses of experimental drug SPC5001, an antisense oligonucleotide directed against PCSK9 (proprotein convertase subtilisin/kexin type 9) that is under investigation as an agent to reduce low-density lipoprotein cholesterol levels. Five days after the last dose, the patient's serum creatinine level increased from 0.81 mg/dL at baseline (corresponding to an estimated glomerular filtration rate [eGFR] of 78 mL/min/1.73 m(2)) to 2.67 mg/dL (eGFR, 20 mL/min/1.73 m(2)), and this increase coincided with the presence of white blood cells, granular casts, and minimal hematuria on urine microscopy. The patient's serum creatinine level peaked at 3.81 mg/dL (eGFR, 13 mL/min/1.73 m(2)) 1 week after the last oligonucleotide dose. Kidney biopsy showed multifocal tubular necrosis and signs of oligonucleotide accumulation. Upon conservative treatment, the patient's serum creatinine level gradually decreased and reached her baseline level 44 days after the last oligonucleotide was administered. The patient recovered fully and kidney function was normal at every follow-up visit.
-
9.
The successful use of vancomycin-impregnated cement beads in a patient with vancomycin systemic toxicity: a case report with review of literature.
Mounasamy, V, Fulco, P, Desai, P, Adelaar, R, Bearman, G
European journal of orthopaedic surgery & traumatology : orthopedie traumatologie. 2013;:S299-302
Abstract
We report the use of vancomycin laden antibiotic cement beads in a patient with calcaneal osteomyelitis who had prior acute kidney injury (AKI). The patient experienced non-oliguric renal failure after exposure to intravenous vancomycin and recovered well after antibiotic discontinuation and adequate hydration. We are not aware of any similar case report where vancomycin laden antibiotic cement has been used in a patient with AKI to vancomycin.
-
10.
Oxalate nephropathy due to 'juicing': case report and review.
Getting, JE, Gregoire, JR, Phul, A, Kasten, MJ
The American journal of medicine. 2013;(9):768-72
Abstract
A patient presented with oxalate-induced acute renal failure that was attributable to consumption of oxalate-rich fruit and vegetable juices obtained from juicing. We describe the case and also review the clinical presentation of 65 patients seen at Mayo Clinic (Rochester, MN) from 1985 through 2010 with renal failure and biopsy-proven renal calcium oxalate crystals. The cause of renal oxalosis was identified for all patients: a single cause for 36 patients and at least 2 causes for 29 patients. Three patients, including our index patient, had presumed diet-induced oxalate nephropathy in the context of chronic kidney disease. Identification of calcium oxalate crystals in a kidney biopsy should prompt an evaluation for causes of renal oxalosis, including a detailed dietary history. Clinicians should be aware that an oxalate-rich diet may potentially precipitate acute renal failure in patients with chronic kidney disease. Juicing followed by heavy consumption of oxalate-rich juices appears to be a potential cause of oxalate nephropathy and acute renal failure.