Herbal medications, such as Tribulus terrestris, are widely used, especially by healthy individuals. Despite being easily accessible and perceived as safe, multiple reports have highlighted the potential adverse effects of these medications, although some acknowledge their benefits. In this case report, we present a 43-year-old male patient who has a significant history of self-administered herbal medicine usage. Our aim is to increase awareness about the potential toxicities linked to the use of over-the-counter herbal medicines. Initially, the patient's elevated creatinine level prompted further investigations, which led to the need for dialysis. Following management, he finally survived and recovered; currently, approximately three months later, the patient remains asymptomatic. This case serves as a cautionary example regarding the potential risks of using herbal medications without proper medical guidance.

[This corrects the article DOI: 10.1371/journal.pone.0342335.].

N-terminal pro-brain natriuretic peptide (NT-proBNP) is secreted by ventricular myocardial cells and released in response to ventricular wall stress conditions such as congestive heart failure (CHF). We previously reported the potential diagnostic efficacy of postmortem urine NT-proBNP concentrations for acute myocardial infarction, CHF, heat stroke, and sepsis. As urine is often unavailable in autopsy cases, alternative diagnostic methods are required. In this study, we conducted NT-proBNP immunostaining of the kidney, evaluated NT-proBNP positivity in the renal tubule in a series of forensic autopsy cases (n = 30), and compared the results to the urinary levels of NT-proBNP and urine Hounsfield unit (HU) values in postmortem computed tomography conducted before the autopsy. The results showed significantly higher urinary NT-proBNP levels in the CHF, sepsis, and heat stroke groups than in the control group. NT-proBNP positivity was also significantly higher in these groups. Moreover, a correlation between urinary NT-proBNP concentration and immunostaining results was observed. These results suggest that NT-proBNP immunostaining of the kidney could be considered as an alternative to NT-proBNP measurement in urine, which may, in turn, improve postmortem diagnosis. However, the association with postmortem urine HU values should be evaluated in further large-scale studies.

Protecting cell/tissue disservice during acute kidney injury (AKI) was an important but still challenging goal. Here, we proposed a current-ultrasound convertion-propelled wireless positioning and tracking nanomachine in which Au covered one side of a PASP-PArg/BaTiO3 footplate (Au@PASP-PArg/BaTiO3, ASPB). These navigational nanomaches were used in the treatment of AKI to confirm a new technology and method for actively inhibiting kidney-trauma formation to enable highly efficient kidney-protection. ASPB possessed the high dielectric constant and piezoelectric properties, which acquired endogenous ultrasound-current and guided navigation under exogenous current excitement. Under the triggering of endogenous ultrasound, ASPB further gave rise to the unbalanced charges on its surface and underwent oxidation-reduction reactions with surrounding water, obtaining H2O2 and [1]O2; meanwhile, ASPB could also decompose water to produce O2 under the inducement of endogenous ultrasound. Additionally, the attained H2O2 and [1]O2 catalyzed polyarginine to discharge NO. Importantly, under accurate navigation, endogenous ultrasound-triggered gas sensor discharged NO/O2, and endogenous current could protect renal tissues from damage based on modulating MYDGF expressions, KCNQ1 functions, and TMAO targeted metabolomics. These current-ultrasound convertion-pushed navigational nanomaches clearly unveiled illustrious potential for promoting highly efficient kidney-function protection.

Iodinated contrast media represent exogenous chemical stressors that can induce renal tubular toxicity, particularly in individuals with pre-existing renal dysfunction. Contrast-induced acute kidney injury (CI-AKI) is increasingly recognized as a form of chemically mediated tubular epithelial cell injury rather than a purely hemodynamic phenomenon. Despite the clinical transition from high-osmolar to low- and iso-osmolar contrast media, nephrotoxicity persists, underscoring the limitations of osmolality-centered paradigms and the need for a mechanistic toxicology framework. This narrative review integrates experimental, translational, and clinical evidence to illuminate the toxicological mechanisms underlying contrast media induced renal tubular epithelial cell (RTEC) injury. By synthesizing classical physicochemical determinants-including osmolality, ionicity, and viscosity-with emerging molecular insights, we identify viscosity-dependent tubular flow perturbation, prolonged intrarenal retention, mitochondrial dysfunction, and oxidative stress as the key upstream toxic events. These converge on a complex network of regulated cell death pathways, including apoptosis, ferroptosis, and pyroptosis, with RTEC as the primary toxicological target. This perspective supports improved understanding of CI-AKI pathogenesis and mechanism-based prevention strategies.

Immunoglobulin A-dominant infection-related glomerulonephritis (IgA-DIRGN) is a rare variant of acute postinfectious glomerulonephritis, typically seen in elderly individuals with comorbid conditions. IgA-DIRGN is characterized by diffuse endocapillary proliferation and the formation of mesangial deposits of IgA and C3, leading to inflammation and subsequently resulting in acute kidney injury, proteinuria, hematuria, and hypocomplementemia. In this report, we describe an immunocompromised 68-year-old man who developed acute kidney injury, nephrotic-range proteinuria, and microscopic hematuria following a splenic Mycobacterium avium abscess. Kidney biopsy showed endocapillary proliferative glomerulonephritis with IgA and C3-dominant granular deposits, consistent with IgA-DIRGN. Progression of kidney dysfunction during antimycobacterial therapy prompted the use of glucocorticoids 1 month after the initial presentation and eventually a splenectomy 1 month later, followed by renal recovery. To our knowledge, this is the first case to report the association between a nontuberculous mycobacterial infection and IgA-DIRGN, emphasizing the importance of source control and illustrating the usefulness of steroids in this patient.

Malakoplakia is a rare chronic inflammatory disease resulting from defective bactericidal activity of macrophages following bacterial infection. The most common causative pathogen is Escherichia coli. This condition predominantly affects immunocompromised individuals, particularly those who have undergone kidney transplantation. Malakoplakia is commonly diagnosed histopathologically based on the presence of Michaelis-Gutmann bodies with typical targetoid structures. In this study, we report a case of malakoplakia caused by Klebsiella pneumoniae in a kidney transplant recipient who presented with a urinary tract infection accompanied by acute kidney injury. To our knowledge, no prior case of renal malakoplakia solely attributed to K pneumoniae in a kidney transplant recipient has been reported. Kidney biopsy revealed numerous periodic acid-Schiff (PAS)-positive globules in the tubulointerstitial area. CD68 immunostaining with PAS counterstain demonstrated that the PAS-positive globules were localized within the cytoplasm of CD68-positive histiocytes (ie, von Hansemann cells). Michaelis-Gutmann bodies were observed using Berlin blue staining. The patient was treated with trimethoprim-sulfamethoxazole, and kidney function stabilized. In kidney transplant recipients, the presence of PAS-positive globules in kidney biopsy specimens should prompt consideration of renal parenchymal malakoplakia in the differential diagnosis. Special stains, such as von Kossa and Berlin blue, are essential for supporting the diagnosis.