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.

Case report: A case of pseudo-acute kidney injury due to cyclin-dependent kinase inhibitor.

Various classes of targeted therapies have emerged in the last few years, which have revolutionized cancer treatment, and improved the prognosis and survival of cancer patients. Unfortunately, these agents have serious toxic effects on the kidneys. Some of the toxic effects are hypertension, acute kidney injury (AKI), and proteinuria. One interesting phenomenon that has emerged recently is pseudo-acute kidney injury due to the interference with the tubular secretion of creatinine by some of the targeted therapeutic agents. Understanding this physiology is needed to avoid unnecessary investigation and withholding of lifesaving chemo regimen. Alternative methods to assess renal function such as cystatin C-based estimated glomerular filtration rate (eGFR) can differentiate true AKI from pseudo-AKI. Here, we describe one such case of pseudo-AKI from cyclin-dependent kinase (CDK) 4/6 inhibitor, abemaciclib, which inhibits tubular secretion of creatinine. Using cystatin-C-based eGFR revealed pseudo-AKI in this case.

Daptomycin-induced hyperkalemia: A case report and brief description of mechanism.

Key Clinical Message: Daptomycin causes serious side effects like rhabdomyolysis at high doses. At lower doses it can cause isolated hyperkalemia without frank rhabdomyolysis. Checking BMP along with CK helps taking timely measures to prevent adverse consequences. Abstract: Hyperkalemia is a common yet challenging clinical condition faced daily by physicians worldwide. Accurate etiology and timely management are paramount in correcting this preventable yet life-threatening electrolyte imbalance. Very seldom has Daptomycin been implicated as a culprit for hyperkalemia. We present one such unique case where a low dose of Daptomycin led to hyperkalemia, and timely identification improved patient outcomes. We present a 69-year-old woman with multiple comorbidities admitted to the intensive care unit to manage diabetic ketoacidosis and sepsis. She developed acute kidney injury due to intravenous contrast, volume depletion, and obstructive uropathy. Interestingly although initially normokalemic, as her renal function started improving with sound urine output, she developed recurrent hyperkalemia, which required medical management. The etiology of hyperkalemia was initially unclear, but on closer review, it was discovered that Daptomycin was the potential culprit. Although case studies with high-dose Daptomycin causing rhabdomyolysis and hyperkalemia have been reported, low-dose Daptomycin causing hyperkalemia without rhabdomyolysis has never been reported, bringing forth the uniqueness of our article.

Infection related membranoproliferative glomerulonephritis secondary to anaplasmosis: A case report.

BACKGROUND: Anaplasmosis is a tick-borne disease with a range of clinical manifestations, from a flu-like illness with fever and myalgias to a severe systemic disease with multisystem organ failure. Although renal involvement is not a common presentation, there have been few cases reporting acute kidney injury from Anaplasmosis. CASE SUMMARY: We present a 55-year-old female with anaplasmosis who developed acute kidney injury due to membranoproliferative glomerulonephritis (MPGN). The patient originally presented with cough and shortness of breath. She was admitted to the hospital with a diagnosis of community acquired pneumonia and received antibiotics. During the hospital course she developed severe acute renal failure. Initial serological work up didn't provide any conclusive diagnosis. Hence, she underwent kidney biopsy which showed MPGN pattern suggesting autoimmune, multiple myeloma or infectious etiology. Extensive work up was undertaken which was negative for autoimmune diseases, vasculitis panel, paraproteinemias but tested positive for IgG anaplasma with high titers indicating Anaplasmosis. CONCLUSION: Our case shows a unique presentation of severe acute renal failure from MPGN from tick borne illness. MPGN is usually seen with autoimmune diseases, hepatitis C virus infections, paraproteinemias. Hence, we suggest that tick borne illness should also be considered when evaluating acute renal failure cases in tick borne prevalent regions.

Acute Myocardial Infarction Caused by Spontaneous Coronary Artery Dissection of the First Septal Perforator.

Spontaneous coronary artery dissection of the septal arteries is rare and may be overlooked on coronary angiogram. Additionally, dedicated intracoronary imaging may not be feasible due to artery size. Cardiac magnetic resonance imaging has an emerging role in diagnosis, which is critical because management changes significantly if spontaneous coronary artery dissection is diagnosed. (Level of Difficulty: Beginner.).

Severe hypernatremia in hyperglycemic conditions; managing it effectively: A case report.

BACKGROUND: Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are common acute complications of diabetes mellitus with a high risk of mortality. When combined with hypernatremia, the complications can be even worse. Hypernatremia is a rarely associated with DKA and HHS as both are usually accompanied by normal sodium or hyponatremia. As a result, a structured and systematic treatment approach is critical. We discuss the therapeutic approach and implications of this uncommon presentation. CASE SUMMARY: A 62-year-old man with no known past medical history presented to emergency department with altered mental status. Initial work up in emergency room showed severe hyperglycemia with a glucose level of 1093 mg/dL and severe hypernatremia with a serum sodium level of 169 mEq/L. He was admitted to the intensive care unit (ICU) and was started on insulin drip as per DKA protocol. Within 12 h of ICU admission, blood sugar was 300 mg/dL. But his mental status didn't show much improvement. He was dehydrated and had a corrected serum sodium level of > 190 mEq/L. As a result, dextrose 5% in water and ringer's lactate were started. He was also given free water via an nasogastric (NG) tube and IV Desmopressin to improve his free water deficit, which improved his serum sodium to 140 mEq/L. CONCLUSION: The combination of DKA, HHS and hypernatremia is rare and extremely challenging to manage, but the most challenging part of this condition is selecting the correct type of fluids to treat these conditions. Our case illustrates that desmopressin and free water administration via the NG route can be helpful in this situation.

Vasopressin-induced hyponatremia in an adult normotensive trauma patient: A case report.

BACKGROUND: Arginine vasopressin is a neuropeptide produced in the hypothalamus and released by the posterior pituitary gland. In addition to maintaining plasma osmolarity, under hypovolemic or hypotensive conditions, it helps maintain plasma volume through renal water reabsorption and increases systemic vascular tone. Its synthetic analogues are widely used in the intensive care unit as a continuous infusion, in addition to hospital floors as an intravenous or intranasal dose. A limited number of cases of hyponatremia in patients with septic or hemorrhagic shock have been reported previously with vasopressin. We report for the first time a normotensive patient who developed vasopressin-induced hyponatremia. CASE SUMMARY: A 39-year-old man fell off a forklift and sustained an axial load injury to his cranium. He had no history of previous trauma. Examination was normal except for motor and sensory deficits. The Imagine test showed endplate fracture at C7 and acute traumatic disc at C7 with cortical degeneration. He underwent cervical discectomy and fusion, laminectomy, and posterior instrumented fusion. After intensive care unit admission post-surgery, he developed hyponatremia of 121-124 mEq/L post phenylephrine and vasopressin infusion to maintain blood pressure maintenance. He was evaluated for syndrome of inappropriate secretion of antidiuretic hormone, hypothyroid, adrenal-induced, or diuretic-induced hyponatremia. At the end of extensive evaluation for the underlying cause of hyponatremia, vasopressin was discontinued. He was also put on fluid restriction, given exogenous desmopressin, and a dextrose 5% in water infusion to prevent osmotic demyelination syndrome caused by sodium overcorrection which improved his sodium level to 135 mmol/L. CONCLUSION: The presentation of vasopressin-induced hyponatremia is uncommon in normotensive patients, and the most difficult aspect of this condition is determining the underlying cause of hyponatremia. Our case illustrates that, considering the vast differential diagnosis of hyponatremia in hospitalized patients, both hospitalists and intensivists should be aware of this serious complication of vasopressin therapy.

Spontaneous Extensive Type A Aortic Dissection in an Older Female with No Risk Factors: A Rare Clinical Presentation.

Background: Aortic dissection (AD) is a rare but serious medical emergency where the aorta's inner layer tears. Females are less likely to develop it than males, and AD cases with unusual symptoms can be hard to diagnose. Diagnosing AD can be further complicated as its symptoms and electrocardiogram (ECG) changes can mimic acute coronary syndrome, and it is challenging to distinguish it without risk factors. Case Report. This case report describes a 60-year-old female patient who presented with unusual symptoms, including pain in her chest, neck, left arm, and lower extremities. An electrocardiogram (ECG) revealed ST elevation in leads aVR and V1, as well as severe ST depression and T wave inversion in the inferior and lateral leads, which can mimic acute coronary syndrome. Despite initial treatment with nitroglycerin, the patient's pain worsened, and a CT angiography revealed type A aortic dissection extending from the aortic root to the right external iliac artery. Immediate surgery was recommended, which significantly improved the patient's condition. Conclusions: Be aware of aortic dissection and its symptoms, even if there are no risk factors or recognizable symptoms. Consider aortic dissection as a potential diagnosis if ECG changes are present. Ongoing education can help decrease mortality and increase awareness.

Effectiveness of Mavrilimumab in Viral Infections Including SARS-CoV-2 Infection - A Brief Review.

Hyperinflammation and cytokine storm has been noted as a poor prognostic factor in patients with severe pneumonia related to coronavirus disease 2019 (COVID-19). In COVID-19, pathogenic myeloid cell overactivation is found to be a vital mediator of damage to tissues, hypercoagulability, and the cytokine storm. These cytokines unselectively infiltrate various tissues, such as the lungs and heart, and nervous system. This cytokine storm can hence cause multi-organ dysfunction and life-threatening complications. Mavrilimumab is a monoclonal antibody (mAb) that may be helpful in some cases with COVID-19. During an inflammation, Granulocyte-macrophage colony-stimulating factor (GM-CSF) release is crucial to driving both innate and adaptive immune responses. The GM-CSF immune response is triggered when an antigen attaches to the host cell and induces the signaling pathway. Mavrilimumab antagonizes the action of GM-CSF and decreases the hyperinflammation associated with pneumonia in COVID-19, therefore strengthening the rationale that mavrilimumab when added to the standard protocol of treatment could improve the clinical outcomes in COVID-19 patients, specifically those patients with pneumonia. With this review paper, we aim to demonstrate the inhibitory effect of mavrilimumab on cytokine storms in patients with COVID-19 by reviewing published clinical trials and emphasize the importance of extensive future trials.