Whether routine antibiotic prophylaxis (AP) should be administered before shockwave lithotripsy (SWL) in patients with sterile urine remains controversial. We aimed to evaluate the effect of AP in this population. We systematically searched Web of Science, Embase, the Cochrane Library, and PubMed through November 20, 2025. The primary outcome was the composite overall infection risk, and secondary outcomes included symptomatic urinary tract infection (UTI), asymptomatic bacteriuria (AB), pyelonephritis, and sepsis. Ten randomized controlled trials involving 3,298 patients were included. AP did not significantly reduce the composite overall infection risk (RR, 0.82; 95% CI, 0.54-1.25; p = 0.35) or AB (RR, 0.80; 95% CI, 0.57-1.13; p = 0.21), but reduced symptomatic UTI (RR, 0.53; 95% CI, 0.29-0.97; p = 0.04). In the only trial reporting pyelonephritis, AP reduced the of pyelonephritis (RR, 0.05; 95% CI, 0.003-0.93; p = 0.04). No sepsis events were reported. Prediction interval and TSA analyses indicated that the symptomatic UTI finding was not definitive. These findings do not support routine universal prophylaxis in all patients with sterile urine undergoing SWL, but may support individualized use in selected patients after considering baseline infection risk, antimicrobial resistance, and antimicrobial stewardship.

IgG4-related disease (IgG4-RD) is a recently described entity comprising pseudo-tumoral and inflammatory conditions that were previously considered separately. It is characterised by specific histological abnormalities, including polyclonal lymphoplasmacytic infiltration, fibrosis and contingent of IgG4+ plasma cells, often associated with elevated serum IgG4 levels and a good response to glucocorticoids. The clinical presentation is highly heterogeneous and requires a multidisciplinary assessment. The diagnosis is based on the identification of suggestive clinical or radiological signs, such as pancreatic, salivary or lacrimal gland involvement, retroperitoneal fibrosis, cholangitis, aortitis, lymphadenopathy or interstitial nephritis. It is also based on the search for laboratory evidence of abnormalities such as polyclonal gammopathy, elevated serum IgG4 levels and complement consumption, and is most often confirmed by organ biopsy. The disease progresses slowly, with gradual symptoms and a risk of sequelae related to fibrosis, particularly pancreatic or renal failure. Management is based on providing the patient with comprehensive information about symptoms, warning signs, adverse events of treatments, vaccination, diet and physical activity. Initial treatment consists of oral glucocorticoids at a dose of 0.4 to 0.6mg/kg/day for two to four weeks, followed by a gradual tapering until discontinuation at three months if possible. This treatment induces remission in more than 90% of cases, but relapses are common, sometimes requiring treatment with immunosuppressants. Follow-up includes regular consultations, imaging tests and laboratory workups, in particular serum IgG4 measurement, in order to monitor disease activity, predict relapses and prevent complications.

Chronic Interstitial Nephritis in Agricultural Communities (CINAC) represents a major public health challenge, primarily affecting young to middle-aged agricultural workers. Clinically, CINAC is characterized by low-grade proteinuria, a bland urinary sediment, and rapidly progressive renal failure. Kidney biopsies disclose large dysmorphic lysosomes containing electron-dense non-membrane aggregates in proximal tubular cells. Although the disease was long attributed to recurrent episodes of dehydration, its pathophysiology is now recognized as more complex. Indeed, the heat-stress hypothesis alone does not adequately explain the heterogeneous geographic distribution of CINAC. Converging epidemiological, environmental, and toxicological evidence suggests a significant role for chronic exposure to pesticides. Several classes of agrochemicals experimentally demonstrated cumulative nephrotoxicity, involving oxidative stress, tubular apoptosis, and mitochondrial and lysosomal dysfunction. The frequent detection of pesticide residues in drinking water and soils within endemic regions indicates chronic low-dose exposure, sometimes independent of direct occupational handling. Heat stress likely acts as a cofactor, amplifying toxicity through dehydration, reduced renal perfusion, and intratubular concentration of toxins. Overall, CINAC appears to result from a multifactorial etiology dominated by exposure to agrochemical mixtures, underscoring the need for integrated and sustainable prevention strategies including depollution and/or reversed osmosis of drinkable water.

Distal renal tubular acidosis (dRTA) is a rare but recognized renal complication of Sjögren's syndrome (SS), often resulting from autoimmune-mediated damage to acid-base transporters in the distal nephron. It commonly presents with electrolyte abnormalities including hypokalemia and metabolic acidosis. A 47-year-old woman with chronic kidney disease presented with recurrent hypokalemia, mild proteinuria, and sicca symptoms. Workup revealed non-anion gap metabolic acidosis, a positive urine anion gap, and renal potassium wasting consistent with dRTA. Autoimmune testing showed a high-titer ANA (1:1280) and elevated SSA (>8.0), confirming SS. Renal biopsy revealed mild interstitial fibrosis and glomerulosclerosis without evidence of tubulointerstitial nephritis or immune complex deposition. This finding supports prior evidence that SS-associated dRTA may occur secondary to functional tubular defects involving distal nephron transporters, even in the absence of overt inflammatory histologic changes. Acid-base disturbances improved with potassium and bicarbonate supplementation. This case highlights that significant tubular dysfunction in SS may occur despite minimal or absent histologic evidence of tubulointerstitial nephritis. dRTA in SS may result from autoimmune targeting of distal nephron transporters such as H⁺-ATPase and anion exchanger 1. Early recognition and supportive treatment are essential to prevent complications including nephrolithiasis, progressive kidney dysfunction, and life-threatening hypokalemia. SS should be considered in patients presenting with unexplained dRTA, and timely correction of electrolyte abnormalities is critical to optimizing outcomes.

Immunoglobulin G4-related disease (IgG4-RD) is a rare chronic immune-mediated multisystem disease with renal manifestations of tubulointerstitial nephritis (IgG4-TIN) and membranous nephropathy (IgG4-MN). IgG4-RD and its sequelae are treated with immunosuppressive therapy, including steroids and rituximab (RTX), which have demonstrated high efficacy in achieving disease remission. We describe a patient who was diagnosed with pancreatitis secondary to IgG4-RD through laboratory and imaging studies. Despite being on RTX, he developed acute kidney injury (AKI) and was diagnosed with IgG4-TIN via kidney biopsy. He was treated with prednisone and RTX, and his symptoms and renal function improved. Despite RTX reaching peak efficacy 6 months after administration, our patient had a breakthrough IgG4-TIN during this period. This case highlights the importance of maintaining a high index of suspicion for renal involvement (IgG4-TIN or IgG4-MN) in patients with AKI superimposed on IgG4-RD, and that maintenance therapy with RTX retreatment was associated with longer relapse-free survival at 12 months of follow-up. Our patient had no severe infections or hypogammaglobulinemia (≤5 g/l) with RTX, confirming RTX's safety and efficacy in maintenance remission therapy for recurrent IgG4-TIN.

Immunoglobulin G4-related disease (IgG4-RD) is a systemic, immune-mediated fibro-inflammatory disorder with the potential to affect multiple organs, with the kidney being the most commonly involved organ, typically presenting as IgG4-related tubulointerstitial nephritis (IgG4-TIN). Anti-neutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis (ANCA-GN), in contrast, is a pauci-immune necrotizing crescentic glomerulonephritis characterized by acute renal dysfunction and systemic inflammation. While early reports have interpreted IgG4-positive plasma cell infiltration in ANCA-associated vasculitis as evidence of overlap with IgG4-TIN, histologic resemblance in varying disease contexts can make differentiation challenging. In this context, we present the case of an 81-year-old woman diagnosed with both ANCA-GN and IgG4-TIN, informed by a comprehensive review of all previously reported cases. Renal biopsy confirmed this rare overlap, revealing pauci-immune crescentic glomerulonephritis alongside dense IgG4-positive plasma cell infiltration and storiform fibrosis. This case illustrates the diagnostic complexity posed by IgG4-rich inflammatory infiltrates in ANCA-associated disease and underscores the importance of careful clinicopathologic correlation to guide accurate diagnosis, appropriate immunosuppressive therapy, and improved understanding of potentially overlapping autoimmune mechanisms.

We report a case of vedolizumab (VDZ)-associated acute interstitial nephritis (AIN) in a 44-year-old man with refractory ulcerative colitis. The case highlights the need for nephrotoxicity monitoring in patients receiving VDZ for inflammatory bowel disease, as well as the inherent difficulties in recognizing AIN in this clinical setting. 4 months after starting VDZ therapy, the patient was admitted with dyspnoea and chest pain. Although investigations for suspected pulmonary embolism were negative, evidence of acute kidney injury was found and a kidney biopsy showed AIN. Identification of the causative role of VDZ was confounded by the fact that the patient was also being treated with omeprazole, which was considered to be the likely cause of AIN. However, rechallenge with VDZ in the absence of omeprazole again led to worsening kidney function that improved when the VDZ was stopped. The presumed recurrence of VDZ-associated AIN occurred during a tapering course of oral prednisolone. This case adds to the literature by reporting detailed tracking of a dechallenge-rechallenge sequence that provides convincing evidence of VDZ-induced AIN. These findings underscore the need for renal surveillance during VDZ therapy to prevent potential progression to chronic kidney disease.