Case Reports in Nephrology最新文献

Background: Nocardia is a gram-positive bacterium capable of causing both local and systemic infections, typically in immunocompromised patients. The most common clinical presentation is pulmonary infection. Muscle abscess due to Nocardia infection without disseminated nocardiosis is rare.

Case report: In this report, we describe the case of a 67-year-old male kidney transplant recipient who developed a swelling of the right biceps muscle. CT imaging showed an intramuscular abscess, which was subsequently surgically drained. The drained fluid grew Nocardia pseudobrasiliensis, which was resistant to imipenem but susceptible to trimethoprim/sulfamethoxazole (TMP-SMX), ciprofloxacin and linezolid. The patient was initially treated with TMP-SMX and ciprofloxacin. Treatment was changed to 6 months of ciprofloxacin and azithromycin due to intolerance to TMP-SMX which resulted in a good clinical response and no recurrence for 3 years. We also review all previously reported N. pseudobrasiliensis infections and cases of nocardiosis presenting as intramuscular infections.

Conclusion: Given its prevalence amongst immunocompromised patients, Nocardiosis requires consideration in the differential diagnosis for the cause of atypical infections in transplant recipients. The antimicrobial susceptibilities of Nocardia are variable depending on species. Of key note, carbapenem resistance has been recently described in N. pseudobrasiliensis. This development should be considered when initiating antimicrobial therapy to ensure good patient response to treatment.

Peritonitis is an important complication of peritoneal dialysis (PD), affecting up to 40% of patients at some point of their PD treatment. Here, we describe a case of PD-associated peritonitis due to an unusual pathogen, Brevibacterium casei. The patient was treated with intraperitoneal antibiotics, successfully preserving the PD catheter. To the best of our knowledge, only four cases of peritonitis due to B. casei have been previously documented worldwide, with catheter preservation achieved in just one other case.

Although the prognosis for patients with ANCA-associated vasculitis (AAV) has improved with modern immunosuppressive drugs, treatment-related complications continue to contribute significantly to morbidity and mortality. Infections, in particular, pose a major risk. Older age, high disease activity at diagnosis, and use of potent immunosuppressants are the most important prognostic factors. Older age is independently associated with mortality, severe renal failure, pulmonary hemorrhage, and relapse. This case highlights the challenge of balancing effective immunosuppression with the associated increased risk of infection. A 77-year-old male treated for MPO-ANCA-positive crescentic glomerulonephritis developed severe complications, including bacteremia, osteomyelitis, and disseminated herpes zoster, ultimately resulting in septic shock. Emerging therapies such as avacopan and predictive tools such as the Death in ANCA Glomerulonephritis-Estimating the Risk (DANGER) score may help clinicians better navigate these complex scenarios by guiding treatment intensity and minimizing risks.

Atypical hemolytic uremic syndrome (aHUS) is a severe condition marked by microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury (AKI). It may result from complement gene mutations or be triggered by other underlying conditions. Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme that protects red blood cells, and its deficiency can cause hemolytic anemia when triggered by certain factors. We report two cases of children diagnosed with G6PD deficiency who initially presented with clinical features of aHUS. In both cases, young boys developed severe AKI and hemolysis, requiring dialysis and treatment with complement inhibitors. A genetic study identified pathogenic mutations in the G6PD gene. Misdiagnosis delayed appropriate management of their underlying condition, highlighting the importance of considering G6PD deficiency in the differential diagnosis of hemolytic anemia, particularly in pediatric patients from high-risk ethnic backgrounds or those with severe hemolysis. To our knowledge, this is the first reported case series in Saudi Arabia linking G6PD deficiency to clinical presentations of aHUS.

Barakat syndrome, also known as HDR syndrome (HDRS), is an autosomal dominant genetic disease classically characterized by hypoparathyroidism (H), deafness (D), and renal disease (R). Less than 200 patients have been reported in the literature since it was first described in 1977 and has meanwhile been shown to have considerable genotypic variability. Barakat syndrome is usually caused by a mutation or knockout in GATA3, a zinc finger protein found on chromosome 10p14 which plays a role in embryologic formation of the central nervous system, thymus, auditory apparatus, kidney, and parathyroid glands. A spectrum of genetic variances in this gene has been related to HDRS, including both noncoding and coding regions with subsequent point mutations, wild-type protein disturbances, and haploinsufficiency. This case presents a 38-year-old female patient with recurrent urinary infections, hearing loss, and chronic kidney disease who underwent extensive laboratory, radiological, and genetic analysis which demonstrated a GATA3 mutation in the 10p15 location. This specific genetic variability is currently absent on the gnomAD database, highlighting the rarity of the mutation. It is crucial to identify rare presentations of Barakat syndrome to allow for the best management, which often revolves around symptomatic management. HDRS prognosis is often determined by the progression of renal disease and thus should be the primary focus of the physician's care of the patient. This case contributes to the body of literature supporting the unique presentation and genetic variability of Barakat syndrome.

Background: Rapidly progressive lupus nephritis (LN) with concurrent positivity for anti-glomerular basement membrane (anti-GBM) antibodies and antineutrophil cytoplasmic antibodies (ANCAs) represents an exceptionally rare and severe autoimmune overlap. Early identification and timely intervention are critical to prevent irreversible renal damage. Case Presentation: A 23-year-old woman with systemic lupus erythematosus presented with acute kidney injury, nephrotic-range proteinuria, pancytopenia, and a SLEDAI score of 41. Serologic tests revealed high-titer anti-GBM antibodies and dual ANCA positivity (MPO and PR3) by the ELISA technique. Although the patient experienced mild hemoptysis and a significant drop in hemoglobin, MSCT of pulmonary vasculature and parenchyma did not reveal alveolar hemorrhage or vascular lesions. Due to contraindications to renal biopsy, she was empirically treated with pulse-dose corticosteroids and plasma exchange, followed by oral corticosteroids and mycophenolate mofetil. Anti-GBM antibodies became undetectable after seven sessions. The patient achieved full clinical, biochemical, and renal remission within 2 months. Conclusion: This case highlights the importance of early serologic evaluation and prompt immunosuppressive therapy in rapidly progressive LN with anti-GBM/ANCA overlap, particularly when histopathological confirmation is not feasible.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are widely used in patients with kidney disease and have been shown to increase serum magnesium levels. Case reports have described their role in correcting hypomagnesemia; however, there is limited evidence regarding their efficacy in patients with renal magnesium wasting. Furthermore, data regarding their role in acute treatment and sustained efficacy to treat hypomagnesemia are lacking. We present a multicenter retrospective, observational case series from two U.S. medical centers describing five patients with refractory hypomagnesemia who experienced significant improvement following initiation of SGLT2 inhibitors. Patients 1-4 showed marked renal magnesium wasting with severe symptomatic hypomagnesemia which responded robustly to SGLT2 inhibitor therapy. Even though Patient 5 did not have renal magnesium wasting, hypomagnesemia still improved with the addition of an SGLT2 inhibitor. Furthermore, the addition of an SGLT2 inhibitor acutely improved the hypomagnesemia of Patients 1 and 2 in an inpatient setting, and Patients 3-5 demonstrated sustained improvement of hypomagnesemia across extended outpatient follow-up. The improvement of hypomagnesemia was irrespective of the diabetic status of the patient. All cases resulted in substantial reduction or cessation of magnesium (Mg) supplementation. These findings suggest a novel therapeutic application of SGLT2 inhibitors for managing intractable hypomagnesemia, both acutely and chronically, regardless of the diabetes being the primary culprit.

Introduction: Renal AA amyloidosis with X-linked hyper-IgM immunodeficiency is rare diseases, and their simultaneous presentation in the same patient is exceptional. Case Presentation: We present a case of renal AA amyloidosis in a 20-year-old man with nephrotic syndrome and reduced glomerular filtration rate (GFR). Clinically, serologically, histopathological, and genetically, we confirm renal amyloidosis in the presence of X-linked hyper-IgM syndrome; in turn, we detected a new hemizygous pathogenic variant in the CD40L gene (c.345delA). Conclusion: Our hypothesis suggests that these conditions predisposed the patient to a combined (cellular and humoral) immunodeficiency, leading to recurrent infectious episodes throughout his life, ultimately resulting in renal amyloidosis due to deposition of serum amyloid protein.

Background: Autosomal dominant polycystic kidney disease (ADPKD) is characterized by diffuse renal cysts that secrete cytokines, which induce interstitial inflammation and fibrosis. Meanwhile, acute tubulointerstitial nephritis (ATIN) is characterized by inflammatory infiltrates in the interstitium, where kidney biopsy remains the mainstay for diagnosis. Case Presentation: An 85-year-old male complained of fatigue, loss of appetite, and low-grade fever for a week. Within the past month, the patient received ciprofloxacin for a urinary tract infection (UTI) and described flu symptoms. The medical history consisted of ADPKD type 2 with baseline serum creatinine (sCr) at 1.2 mg/dL. Labs showed acute kidney injury (AKI) (sCr = 3.98 mg/dL). The combination of previous drug and infection exposure, systemic symptoms, and AKI suggested the diagnosis of ATIN. The kidney function and clinical status improved with corticosteroids (CS) treatment, where sCr returned to 2.4 mg/dL. Unfortunately, the patient died due to severe community-acquired pneumonia. Conclusion: This case highlighted the dilemma of ATIN diagnosis in a patient with ADPKD and presents the first case of ATIN in ADPKD patients. Kidney biopsy was unable to be performed for ATIN diagnosis in this ADPKD patient due to diffuse renal cysts. Also, the biopsy could be confused by interstitial fibrosis and infiltrates that appeared early in ADPKD biopsies. Clinicians could suggest an ATIN diagnosis and start treatment based on the combination of new-onset AKI aligned with clinical history and laboratory tests in such ADPKD patients. Also, the improvement of kidney function after CS treatment could support the ATIN diagnosis.

Acute kidney injury is a potentially fatal condition, particularly in low-resource settings, where access to renal replacement therapy is limited. This creates a problem of accessibility to healthcare for many patients living in low-resource settings. A 10-year-old boy in rural Ghana presented with anuria, edema, hypertension, and seizures, and severely elevated creatinine and urea levels were measured. Local peritoneal dialysis was started on Day 4 of admission, and the patient showed significant improvement. This report shows the effectiveness including subsequent laboratory results of locally made peritoneal dialysis and gives a detailed description on how to locally make dialysis fluids and how to perform peritoneal dialysis in a low-resource setting.