Collagen type III glomerulopathy is a rare glomerular disorder characterized by the deposition of type III collagen fibers within the glomeruli, predominantly in the mesangial and subendothelial regions. Renal biopsy with histopathological examination remains the gold standard for diagnosis of this disease. Clinically, collagen type III glomerulopathy typically presents with proteinuria and progressive renal dysfunction, with or without nephrotic syndrome. Collagen type III glomerulopathy affects individuals across all age groups, ranging from children to adults, and shows no apparent sex predominance. This study retrospectively analyzed four patients with collagen type III glomerulopathy diagnosed at the First Affiliated Hospital of Wenzhou Medical University between 2011 and 2024 and reviewed 105 cases reported worldwide in the English-language literature. All patients presented with proteinuria, and half had renal impairment. Electron microscopy consistently demonstrated abnormal collagen fibrils in the mesangial region. Over a median follow-up of 71.5 months, half of the patients with available follow-up data progressed to end-stage renal disease, whereas the remaining patients maintained stable renal function after intervention. Globally, reported collagen type III glomerulopathy cases exhibited heterogeneous clinical presentations, and current data support an association between nephrotic-range proteinuria and poorer renal outcomes.

Solitary functioning kidney (SFK) is a clinical condition characterized by the presence of a single functioning kidney, arising from either congenital anomalies or acquired causes. It is recognized as an important risk factor for chronic kidney disease (CKD) and, in some patients, for progression to end-stage kidney disease (ESKD). Congenital solitary functioning kidney is commonly associated with renal hypoplasia or dysplasia, genetic abnormalities, and congenital anomalies of the kidney and urinary tract, whereas acquired solitary functioning kidney is often secondary to unilateral nephrectomy for renal tumors, trauma, tuberculosis, severe infection, or living kidney donation. The principal pathophysiological mechanisms underlying the progression from SFK to CKD are compensatory renal hypertrophy and glomerular hyperfiltration in the remnant kidney. Although these adaptive responses may initially maintain renal function, sustained compensation can lead to glomerular injury, proteinuria, tubulointerstitial damage, and renal fibrosis. Early diagnosis relies primarily on imaging modalities, such as ultrasonography and magnetic resonance imaging, together with assessment of renal function and emerging biomarkers, including neutrophil gelatinase-associated lipocalin and cystatin C. Prognostic evaluation of patients with SFK should comprehensively consider etiology, age, compensatory renal growth, associated urinary tract anomalies, comorbidities, and markers of kidney injury. Effective long-term management is essential to prevent or delay progression to CKD and ESKD, with particular emphasis on individualized follow-up, lifestyle modification, blood pressure control, reduction of proteinuria, and avoidance of additional nephrotoxic insults. Previous publications have often addressed pediatric congenital solitary functioning kidney (CSFK), living kidney donors, and disease-related nephrectomy cohorts separately, limiting the translation of heterogeneous evidence into a common clinical approach. This review integrates congenital and acquired SFK across the life course, distinguishes shared markers of established kidney injury from etiology-specific determinants of renal reserve, and proposes an evidence-informed framework for dynamic risk stratification and risk-adapted follow-up and management. This framework is conceptual and requires prospective validation.

Proteinuria, defined by an abnormally elevated concentration of proteins in the urine, serves as a critical biomarker for the early detection and diagnosis of preeclampsia. Elevated proteinuria levels adversely affect both maternal and foetal health, increasing the risk of preterm birth and low birth weight. This study focused on the identification of proteinuria in blood samples through Fourier-transform infrared (FTIR) spectroscopy as a diagnostic tool for real-time diagnosis. Blood plasma collected during birth was evaluated in four study groups: pregnant controls (n = 12), pregnant women with proteinuria (n = 13), newborn controls (n = 12), newborns with proteinuria (n = 14). First, attenuated total reflectance-FTIR spectra of plasma samples were collected for subsequent spectral smoothing, vector normalisation and machine-learning classification with various supervised machine learning algorithms, including several types of Support Vector Machine, K-Nearest Neighbours and decision trees. We obtained (76.1 ± 3.1)% accuracy, (72.1 ± 4.8)% sensitivity and (80.4 ± 3.8)% specificity for pregnant classification, and (90.6 ± 1.5)% accuracy, (83.3 ± 2.4)% sensitivity and (98.9 ± 1.6)% specificity for newborn classification. The vibrational modes corresponding to the predominant biochemical components in blood plasma of pregnant women and newborns were listed. Sensitivity and specificity results demonstrated that FTIR can be a promising tool for early diagnosis and monitoring of individual proteinuria. Although the proposed spectroscopic approach demonstrated promising diagnostic performance, the findings should be interpreted in light of clinical conditions that could affect the biochemical profile. Further studies involving larger and more heterogeneous populations are required to validate the proposed methodology.

A 14-year-old male was admitted with a three-month history of fever and eyelid erythema and edema. The clinical course was notable for progressive weight loss, livedo reticularis, and multiple lymph node enlargements. Laboratory investigations revealed negative antinuclear antibodies,significantly reduced complement levels, positive anticardiolipin antibodies, hemolytic anemia, and proteinuria. Imaging studies demonstrated pulmonary inflammation, intracranial venous sinus thrombosis, and pericardial effusion. Based on a comprehensive assessment, the patient was diagnosed with systemic lupus erythematosus (antinuclear antibodies-negative), complicated by antiphospholipid syndrome and cerebral venous sinus thrombosis. Initial management included pulse steroid therapy, intravenous immunoglobulin, immunosuppressive agents, and heparin anticoagulation, which resulted in transient clinical improvement. During hospitalization, the patient developed acute intracranial hemorrhage, necessitating emergent surgical decompression and therapeutic adjustment. Subsequently, an active pulmonary infection emerged and was treated with antimicrobial therapy alongside Pneumocystis jirovecii pneumonia prophylaxis, leading to stabilization of his condition.This case underscores several key considerations: (1) the diagnostic complexity of childhood SLE, particularly in ANA-negative cases, which requires integration of clinical and extensive immunologic profiling; (2) the importance of testing for non-criteria antiphospholipid antibodies in suspected antiphospholipid syndrome; (3) the fact that cerebral venous sinus thrombosis is a rare but severe complication in which anticoagulation must be carefully balanced against the risk of hemorrhage; and (4) the critical need for vigilant infection prevention, proactive management, and close monitoring of drug-related toxicities. A multidisciplinary approach is essential to tailor individualized treatment strategies and optimize patient outcomes.