Background and Objectives: Nutritional status is essential for outcomes in hemodialysis (HD) patients. Incremental HD (iHD) may help preserve residual renal function, but its effect on nutrition and body composition is unclear. Nutritional ultrasound (NUS) offers a non-invasive way to assess muscle and fat, complementing methods like BIA. This study compared nutritional status using morphofunctional assessment in patients on iHD versus conventional HD (cHD). Material and Methods: This single-center observational cross-sectional study included 74 stable adult HD patients (>3 months). Patients were stratified into iHD (n = 13; 1–2 sessions/week) and cHD (n = 61; 3 sessions/week). Evaluations included clinical and biochemical parameters, BIA, handgrip strength, nutritional scores and NUS assessed mass muscle of anterior quadriceps rectus femoris (QRF), supramuscular fat (SMF), subcutaneous adipose tissue (SAT), and preperitoneal visceral fat (PPVF). Results: Patients on iHD exhibited a more favorable nutritional and inflammatory profile, with a lower risk of malnutrition and a reduced prevalence of protein-energy wasting (PEW) syndrome. Although BIA failed to clearly differentiate between groups, NUS identified better preservation of SMF in iHD patients (8.3 ± 2.5 vs. 6.6 ± 2 mm; p = 0.009), as well as higher preperitoneal visceral fat thickness (1.9 ± 4.9 vs. 0.6 ± 0.3 cm; p = 0.04). There was also a trend toward greater muscle thickness in the iHD group, such as the Y-axis (9.5 ± 2 vs. 8.5 ± 2.3 mm; p = 0.17) and cross-sectional area muscle of rectus femoris (CS-MARF in cm²) (2.9 ± 0.6 vs. 2.6 ± 0.8 mm; p = 0.1) of anterior QRF, although without reaching statistical significance. Conclusions: These results highlight the value of NUS as a sensitive method for assessing nutritional status in HD patients, particularly within individualized strategies such as iHD, where it may provide key complementary information not captured by conventional methods.

Background: Fibrillary glomerulonephritis (FGN) is a rare and poorly understood kidney disease characterized by the deposition of non-amyloid fibrils in the glomeruli. Its clinical heterogeneity and high rate of progression to end-stage renal disease (ESRD) pose significant diagnostic and therapeutic challenges. This case series aims to enhance awareness of FGN and emphasizes the need for further research to improve patient outcomes. Case Reports: We reviewed the clinical, histopathological, and therapeutic data of three patients with FGN diagnosed by kidney biopsy. The cases included variations in clinical presentation from nephrotic syndrome to rapidly progressive glomerulonephritis (RPGN). Diagnostic methods incorporated light microscopy, immunofluorescence, and electron microscopy, with the integration of DnaJ homolog subfamily B member 9 (DNAJB9) staining for confirmation. Patient 1 showed a more favorable response to rituximab, achieving complete remission (CR) at 6 months and maintaining CR after 3 years. Patient 2 showed only partial remission after 2 years following treatment with rituximab. Patient 3 presented with RPGN and rapidly progressed to ESRD despite aggressive immunosuppressive therapy. Discussion: DNAJB9 has emerged as both a specific and sensitive biomarker in patients with FGN and has facilitated accurate differentiation from other glomerulopathies. This series underscores the variability in clinical outcomes and responses to therapy as well as the importance of early and accurate diagnosis. Conclusions: FGN remains a diagnostic and therapeutic challenge due to its rarity and heterogeneity. Advances in biomarkers like DNAJB9 have improved diagnostic accuracy, distinguishing FGN from similar conditions such as immunotactoid glomerulopathy. Further research into pathophysiological mechanisms and targeted therapies is essential to optimize management and outcomes for affected patients.

Background: Lupus podocytopathy (LP) is a non-immune complex-mediated glomerular lesion in systemic lupus erythematosus (SLE), characterized by the diffuse effacement of podocyte processes without immune complex deposition or with only mesangial immune complex deposition. LP is a rare cause of nephrotic syndrome in SLE patients with implications for prognosis and treatment. Case Report: We present the case of a 28-year-old woman with a medical history of type 1 diabetes mellitus (T1DM) who presented with lower limb edema, dyspnea, hypercholesterolemia, with nephrotic range proteinuria, without acute kidney injury, and laboratory findings compatible with auto-immune hemolytic anemia. They had negative infectious serology, positive antinuclear antibody (ANA), and an eye fundus examination showing diabetic retinopathy. A biopsy was performed to define the etiology of the renal involvement, which was compatible with LP. Following immuno-suppressive and antiproteinuric therapy, the patient evolved with the complete remission of the nephrotic syndrome. Conclusions: Lupus podocytopathy is an infrequent anatomopathological entity, so this case is presented as the first reported in Peru, and a literature review is made.

Background/Objectives: Acetazolamide is widely used for acute mountain sickness (AMS) prophylaxis. Whilst generally safe, acute kidney injury (AKI) is a rare but serious adverse event. We present a case of anuric AKI following minimal exposure to acetazolamide, contributing to the limited literature on its nephrotoxicity at prophylactic doses. Methods: A 54-year-old previously healthy male ingested 250 mg/day of oral acetazolamide for two days. He developed acute anuria and lumbar pain. Diagnostic evaluation included laboratory tests, imaging, microbiological cultures, autoimmune panels, and diuretic response. No signs of infection, urinary tract obstruction, or systemic disease were found. Results: The patient met KDIGO 2012 criteria for stage 3 AKI, with peak serum creatinine of 10.6 mg/dL and metabolic acidosis. Imaging confirmed non-obstructive nephrolithiasis. Conservative treatment failed; intermittent hemodialysis was initiated. Renal function recovered rapidly, with the normalization of serum creatinine and urinary output by day 4. Conclusions: This case represents the lowest cumulative dose of acetazolamide reported to cause stage 3 AKI. The findings support a pathophysiological mechanism involving sulfonamide-induced crystalluria and intratubular obstruction. Physicians should consider acetazolamide in the differential diagnosis of AKI, even with short-term prophylactic use.

Background and Clinical Significance: Membranoproliferative glomerulonephritis (MPGN) is a rare and heterogeneous pattern of immune-mediated glomerular injury, often associated with infections, autoimmune disorders, or monoclonal gammopathies. Idiopathic cases remain a diagnostic challenge and frequently require empirical immunosuppressive treatment. There is increasing interest in environmental triggers that may activate the immune system in genetically or immunologically predisposed individuals. We report an unusual case of idiopathic immune complex-mediated MPGN with a relapsing course potentially associated with vaccine-induced immune reactivation. Case Presentation: A 35-year-old male with no significant medical history aside from untreated dyslipidemia and active smoking presented with a hypertensive emergency and acute kidney injury (AKI). Laboratory investigations revealed nephrotic-range proteinuria, microscopic hematuria, and reduced estimated glomerular filtration rate (eGFR). Kidney biopsy demonstrated type I immune complex-mediated MPGN with a diffuse endocapillary proliferative pattern and granular subendothelial deposits (IgG+++, C3+++, C1q++). An extensive work-up ruled out secondary causes, supporting a diagnosis of idiopathic MPGN. Immunosuppressive therapy with corticosteroids and mycophenolate mofetil led to a partial clinical response. However, after receiving multiple vaccinations, the patient experienced clinical deterioration. A second biopsy revealed persistent proliferative changes and new deposits of IgM++, C4d++, and both kappa and lambda light chains. This prompted a reintroduction of immunosuppressive therapy, which resulted in subsequent clinical improvement. Conclusions: This case supports the hypothesis that vaccine-induced immune reactivation may serve as a potential trigger for disease relapse in idiopathic MPGN. Clinicians should remain alert to environmental stimuli that may influence disease activity in immune-mediated glomerulopathies. Further research is needed to elucidate the underlying immunopathogenic mechanisms.

Background: Fluid accumulation syndrome (FAS) is a well-recognized predictor of adverse outcomes in critically ill patients, particularly in the context of sepsis and cardiorenal syndrome. However, extreme cases of fluid accumulation exceeding 60 L are rare and poorly described. We report a unique case of severe, multifactorial congestion and discuss the diagnostic and therapeutic challenges, including the role of bedside ultrasound and venous congestion assessment, as well as the importance of bioelectric impedance analysis (BIA) for patient monitoring and follow-up. Case Presentation: We describe the clinical course of a 51-year-old male with dilated cardiomyopathy and infectious endocarditis who underwent tricuspid valve surgery complicated by cardiogenic and septic shock. The patient developed progressive congestion despite maximal medical management. Serial BIA and venous excess ultrasound (VExUS) assessments were used to monitor venous congestion and guide renal replacement therapy (RRT). A targeted literature review was performed to contextualize this case within current evidence on FAS and Compartment Balance Disorder in Intensive Care Units (CBD-ICUs). Results: The patient accumulated over 68 L of positive fluid balance due to prolonged vasopressor support, multiorgan failure, nutritional and infectious complications. Continuous and then intermittent hemodiafiltration, guided by point-of-care ultrasound and BIA, allowed gradual decongestion. Renal function recovered, and ventilator support was weaned after 120 days in intensive care. The literature review highlighted the prognostic relevance of FAS and emerging tools such as BIA and VExUS for individualized fluid management. Conclusions: Extreme FAS may reflect a failure of systemic and compartmental fluid regulation in critically ill patients (CBD-ICU). VExUS-guided decongestion, BIA and early RRT may improve outcomes in complex scenarios of overlapping cardiorenal and septic syndromes.