Search Results (197)

Objectives: Aspidopterys obcordata has been traditionally used by the Dai people in Xishuangbanna, China, for the prevention and treatment of renal calculi. This study aimed to investigate the inhibitory effect of A. tomentosa extracts on calcium oxalate stone formation. Methods: The extracts of A. tomentosa (EA) were obtained via 95% ethanol reflux extraction, followed by multi-polar solvent extraction and elution. The HK-2 cell injury model induced by calcium oxalate and the renal calculus mouse model established by intraperitoneal injection of glyoxylic acid were established to assess drug efficacy. EA intervention was performed to evaluate its effects on calcium oxalate crystal deposition, renal tubular injury, cell apoptosis, and serum creatinine (Scr) and blood urea nitrogen (BUN) levels. Furthermore, the potential mechanism underlying, particularly the regulation of PERK/ATF4/CHOP signaling pathway and endoplasmic reticulum stress-mediated apoptosis, was investigated. Results: EA treatment significantly reduced renal calcium oxalate crystal deposition, alleviated renal tubular injury, inhibited cell apoptosis, and decreased Scr and BUN levels. Mechanistically, the protective effects of EA were mediated by the downregulation of the PERK/ATF4/CHOP signaling pathway and the suppression of endoplasmic reticulum stress-mediated apoptosis. Conclusions: These findings provide experimental evidence supporting that A. tomentosa can be developed as a promising agent for the prevention of nephrolithiasis. Full article

Background: Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome caused by fibroblast growth factor 23 (FGF-23)-secreting tumors, typically of mesenchymal origin, leading to renal phosphate wasting and severe bone demineralization and fragility fractures. Diagnosing TIO remains a significant clinical challenge, particularly when coexisting mineral metabolism disorders, such as hypercalcemic hyperparathyroidism, are masking its clinical presentation. Case Presentation: A 74-year-old woman with fragility fractures, generalized bone pain, and nephrolithiasis was initially diagnosed with primary hyperparathyroidism due to concomitant hypercalcemia, hypophosphatemia, and elevated parathyroid hormone (PTH). Despite a successful parathyroidectomy, which normalized calcium levels, severe hypophosphatemia persisted due to renal phosphate wasting. High FGF-23 levels and subsequent functional imaging indicating a somatostatin receptor-positive lesion in the left popliteal fossa led to the diagnosis of TIO. Surgical resection immediately normalized FGF-23 levels, leading to a slower rise in phosphorus during follow-up. Histopathology revealed a tophaceous-like giant cell granulomatous reaction, recalling the earlier report by Prader. Conclusions: This case highlights that parathyroid disorders can coexist with TIO, and they may delay its diagnosis. In this circumstance, a high index of clinical suspicion is represented by the persistence of hypophosphatemia post-parathyroidectomy. Full article

Background and Objectives: Multidrug-resistant (MDR) uropathogens are reshaping the empirical management of acute pyelonephritis, particularly in Eastern European centers. We aimed to describe MDR patterns, identify admission-level predictors, including renal impairment/renal-failure status at presentation and major healthcare exposure variables, and derive a bedside risk score (PYELO-MDR-Risk) for adult pyelonephritis at a Romanian tertiary hospital. Methods: We retrospectively analyzed 129 consecutive culture-confirmed acute pyelonephritis admissions at “Victor Babeș” University Hospital, Timișoara (March 2022–March 2025). MDR was defined as non-susceptibility to ≥1 agent in ≥3 antimicrobial categories. We compared MDR and non-MDR cases on demographics, microbiology, time-to-effective therapy (TTE), and outcomes; multivariable logistic regression identified independent predictors and was the basis for a points-based score with bootstrap-based internal validation (1000 resamples). Results: Fifty-four patients (41.9%) had MDR pyelonephritis. Escherichia coli remained the dominant uropathogen (55.8%) but was less prevalent in the MDR group (40.7% vs. 66.7%; p = 0.003), whereas Klebsiella pneumoniae and Pseudomonas aeruginosa were enriched. Independent predictors of MDR were antibiotic exposure ≤90 days (aOR 5.7, 95% CI 2.4–13.6), recurrent UTI (aOR 3.4, 1.4–8.2), recent hospitalization (aOR 3.1, 1.2–8.0), and renal impairment/renal-failure status at admission (aOR 2.4, 1.0–6.2). Immunosuppression, prior urinary tract instrumentation, and nephrolithiasis/urolithiasis were evaluated as candidate predictors but did not independently improve the final point score after adjustment. MDR was associated with delayed effective therapy (28.4 vs. 9.7 h; p < 0.001), longer hospitalization (13.7 vs. 8.9 days; p < 0.001), and higher 30-day readmission (20.4% vs. 8.0%; p = 0.038). The PYELO-MDR-Risk score (range 0–12) achieved an optimism-corrected AUC of 0.84 with adequate calibration (Hosmer–Lemeshow p = 0.624). Conclusions: MDR drives a substantial fraction of pyelonephritis admissions in Western Romania and tracks closely with prior antibiotic and healthcare exposure. The PYELO-MDR-Risk score offers a transparent bedside tool for empirical-therapy decisions in the local setting, pending national and international external validation. Full article

Inflammatory bowel disease (IBD), comprising Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic relapsing–remitting condition characterized by systemic and intestinal inflammation and immune dysregulation. Up to 47% of IBD patients develop extraintestinal manifestations, yet kidney and urological involvement remain underrecognized. Accumulating evidence has linked IBD to nephrolithiasis, glomerular diseases, tubulointerstitial nephritis, acute kidney injury, chronic kidney disease, and, rarely, amyloid A amyloidosis. Population studies have consistently shown elevated risks for various important kidney disorders in IBD, with CD generally posing a greater risk than UC. The pathogenesis of kidney complications in IBD reflects complex gut–kidney interactions, including metabolic and absorptive abnormalities, shared genetic and immune pathways, intestinal dysbiosis with nephrotoxic microbial metabolites, systemic inflammation, and drug-related nephrotoxicity. Strategies for kidney protection in IBD include increased awareness, close monitoring of kidney function, urinary metabolic profiling in high-risk patients, and prompt nephrology referral for early detection and treatment. Management should include an effective and sustained control of intestinal inflammation, discontinuation of potential nephrotoxic drugs when indicated, and timely diagnosis and treatment of kidney manifestations, as well as integrating kidney complications into IBD guidelines to enhance awareness, ultimately optimizing both the kidney and overall outcomes for IBD patients. Future studies are needed to validate the potential predictive biomarkers for kidney complications and to develop targeted interventions to address shared gut–kidney pathogenic mechanisms in IBD. Full article

Background: Primary hyperparathyroidism (PHPT) has undergone notable clinical changes over recent decades, with asymptomatic cases now prevailing in Western countries. In contrast, a broad spectrum of clinical manifestations remains common in Romania, an Eastern European country. This study aims to provide a representative descriptive analysis of clinical presentations and related complications observed in this setting. Methods: We performed a cross-sectional, single-center study of 413 consecutive PHPT cases diagnosed between 2000 and 2020 at a tertiary endocrinology center in Romania. Data included demographics, clinical features, biochemistry, bone turnover markers, 25OHD, BMD by DXA, TBS, fractures, renal involvement, and etiology. Results: Patients were predominantly female (88.6%), with a mean age of 60 ± 11.7 years and a mean BMI of 27.3 ± 5.7 kg/m². Familial forms were identified in 4.4%. Mean serum calcium was 11.28 ± 1.09 mg/dL, mean PTH 248.31 ± 361.94 pg/mL, and mean 25OHD 17.95 ± 9.6 ng/mL. Symptomatic hypercalcemia was present in 23.2% and severe vitamin D deficiency in 21%. Fractures were present in 25.2% and osteitis fibrosa cystica in 1.7%. Mean T-scores (SD): LS –2.23, FN –1.85, 1/3 distal radius –1.96. Osteoporosis prevalence: LS 47%, FN 24.1%, 1/3 distal radius 38%. Mean TBS was 1.258 ± 0.115. Renal involvement included calcifications (56.7%), nephrolithiasis (53%), nephrocalcinosis (3.6%), hypercalciuria (31.7%), and reduced renal function (9.93%). Non-classical manifestations were mainly cardiovascular (58%) and osteoarticular (24.5%). Parathyroidectomy was performed in 217 patients (53%); histopathology showed adenoma (88.8%), carcinoma (5.2%), and hyperplasia (6%), with a mean adenoma weight of 2.86 ± 5.92 g. Conclusions: PHPT in Romania shows a heterogeneous phenotypic spectrum, reflecting variability in clinical presentation and suggesting an evolving epidemiological profile. Full article

Hyperoxaluria Type 1 (PH1) is a rare autosomal recessive metabolic disorder caused by mutations in the AGXT gene, leading to impaired glyoxylate metabolism and excessive oxalate accumulation, resulting in nephrolithiasis, nephrocalcinosis, and end-stage renal disease. As a rare and often neglected disease, PH1 poses a significant challenge to modern healthcare systems due to its progressive nature and limited therapeutic options. In this study, an integrated in silico approach was employed to identify pathogenic single-nucleotide polymorphisms (SNPs) and evaluate potential therapeutic candidates. Computational analyses using ConSurf, Align-GVGD, INPS-MD, CUPSAT, and iStable identified G161C and Y260C as highly deleterious variants affecting protein stability. Virtual screening, followed by ADME and toxicity assessments, identified Tauroursodeoxycholic acid (TUDCA) as a promising candidate with favorable pharmacokinetic and safety profiles. Molecular docking revealed that TUDCA exhibited higher binding affinity than the reference drug pyridoxine across native and SNP variants of AGXT proteins. Molecular dynamics simulations (300 ns) demonstrated enhanced structural stability of TUDCA-bound complexes, indicated by reduced RMSD and RMSF, improved compactness, and sustained hydrogen bonding. Furthermore, free energy landscape (FEL) and dynamic cross-correlation matrix (DCCM) analyses confirmed improved conformational stability and coordinated residue motions in SNP variant structures. Overall, these findings suggest that TUDCA may effectively stabilize structural alterations induced by pathogenic AGXT variants, highlighting its potential as a precision medicine-based therapeutic strategy for PH1. Full article

Background/Objectives: Urinary calcium excretion is a key parameter in assessing mineral metabolism and diagnosing conditions such as nephrolithiasis, osteoporosis, and hyperparathyroidism. The 24 h urine collection is the gold standard for evaluating calcium excretion, but it is often impractical due to patient non-compliance and logistical challenges. As an alternative, the calcium-to-creatinine ratio (CCR) in spot urine has been proposed, although its reliability remains debated. This study aims to systematically compare the calcium levels in spot urine samples with those obtained from 24 h urine collections to assess their agreement and clinical applicability. Methods: This retrospective, multi-center study analyzed data from 201 patients who provided both 24 h and spot urine samples during routine diagnostic work-up between 1 January 2019 and 31 December 2024. Calcium excretion was normalized using the calcium-to-creatinine ratio (CCR). The agreement between the two methods was assessed using Bland–Altman analysis, Pearson and Spearman correlation coefficients, and receiver operating characteristic (ROC) curve analysis. Results: Hypercalciuria, defined as ≥6.25 mmol/24 h in women and ≥7.5 mmol/24 h in men, was detected in 52.7% of cases based on 24 h urine. ROC analysis showed that spot urine CCR had moderate diagnostic accuracy (AUC = 0.76). The optimal cut-off for predicting hypercalciuria was 4.4 mmol/g (sensitivity 70.8%, specificity 72.4%). Overall agreement between spot urine CCR and 24 h urine CCR was moderate, with a Bland–Altman geometric mean ratio of 1.06 and multiplicative limits of agreement of 0.59 to 1.91. A low spot urine CCR below 2 mmol/g showed high sensitivity but low specificity and had a negative predictive value of 82%. Conclusions: Spot urine CCR cannot replace 24 h urine collection for accurately assessing urinary calcium excretion, but very low values may have limited utility as an initial rule-out tool in selected patients. Very low spot urine CCR values may help rule out hypercalciuria in a limited subgroup of patients and may therefore support triage decisions in selected clinical situations. Further prospective studies are needed to validate these findings. Full article

Kidney stone disease is a common urinary system disorder with a continuously rising global incidence, posing a major public health challenge. As a classic traditional Chinese medicine for the treatment of kidney stones, Lysimachia christinae Hance (LCH) has not yet been fully elucidated in terms of its pharmacological mechanism. In this study, a rat model of calcium oxalate kidney stones and a calcium oxalate monohydrate (COM)-induced injury model of human renal tubular epithelial (HK-2) cells were established. Combined with transcriptomic analysis and experimental verification, the therapeutic effect and underlying molecular mechanism of LCH against kidney stones were systematically explored. Results demonstrated that LCH extract significantly reduced serum levels of blood urea nitrogen (BUN) and creatinine (Cr), as well as renal tissue levels of kidney injury molecule-1 (KIM-1) and cystatin-C (Cys-C) in rats with calcium oxalate crystal-induced renal injury, and diminished calcium oxalate crystal deposition and adhesion in rat renal tissues as well as HK-2 cells, thus exerting a robust renoprotective effect. Mechanistically, transcriptome sequencing indicated that the anti-nephrolithiasis effect of LCH was closely related to the inhibition of oxidative stress and ferroptosis. LCH extract reversed CaOx crystal-induced upregulation of NADPH oxidase 2 (NOX2) and downregulation of superoxide dismutase 2 (SOD2), reduced intracellular oxygen species (ROS) levels, downregulated the expression of transferrin receptor 1 (TFR1) and acyl-CoA synthetase long-chain family member 4 (ACSL4) while upregulating that of ferritin heavy chain 1 (FTH1), solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4), and diminished intracellular iron accumulation, thereby effectively ameliorating crystal-mediated renal injury. The present study demonstrates that the therapeutic effect of LCH on kidney stones is closely related to the regulation of the NOX2/ROS signaling axis and ferroptosis, providing novel theoretical evidence for its clinical application. Full article

Background/Objectives: Acute kidney injury (AKI) is a clinically important complication among hospitalized urology patients. However, data from general urology inpatient populations remain limited. We aimed to assess AKI frequency in a monitored urology inpatient cohort, identify associated predictors, and develop an exploratory admission-based risk stratification model. Methods: We conducted a retrospective observational cohort study of adults admitted to a tertiary urology ward between June 2023 and May 2024 who had at least two serum creatinine measurements during hospitalization. AKI was defined according to Kidney Disease: Improving Global Outcomes (KDIGO) serum creatinine criteria. Demographic, clinical, laboratory, and procedural data were analyzed. Multivariable logistic regression identified factors associated with AKI and was used to construct a reduced exploratory admission-based risk model. Results: Among 196 monitored patients, 67 (34.2%) developed AKI during hospitalization, and 82.1% had KDIGO Stage 1 AKI. Higher admission serum creatinine, hypertension, nephrolithiasis, and ureteral interventions were independently associated with AKI. AKI was also associated with longer hospitalization (6.4 ± 4.2 vs. 5.1 ± 3.2 days, p = 0.044). The reduced exploratory model identified low-, intermediate-, and high-risk groups with progressively increasing AKI incidence (7.7%, 32.3%, and 76%, respectively; AUC = 0.76). Conclusions: In this monitored cohort, AKI was frequent and associated with admission characteristics and prolonged hospitalization. These findings support targeted renal monitoring in higher-risk patients. The admission-based risk model is exploratory and requires validation in prospective multicenter cohorts before clinical implementation. Full article

Hereditary renal tubulopathies are rare monogenic disorders caused by defects in tubular transport mechanisms that impair the handling of electrolytes, water, and acid–base balance along the nephron. While each tubulopathy is individually uncommon, their collective burden is clinically relevant, as these disorders can severely affect quality of life and predispose to nephrolithiasis, dehydration episodes, and progression to chronic kidney disease. Advances in molecular genetics have identified more than 70 genes involved in renal tubular physiology; however, a substantial proportion of these cases remain genetically unresolved, and marked phenotypic heterogeneity complicates diagnosis and management. This narrative review provides an integrated overview of the main transport systems operating in the different tubular segments of the nephron—proximal tubule, thick ascending limb of the loop of Henle, distal convoluted tubule and collecting duct—summarizing the tubulopathies associated with each segment and discussing in greater detail representative inherited disorders that illustrate the clinical consequences of their dysfunction. We highlight current diagnostic challenges and limitations of existing therapeutic strategies and discuss novel diagnostic approaches as well as emerging treatment options. Improved genetic diagnosis, validation of candidate biomarkers, and the development of novel therapeutic strategies will be essential to advance precision medicine and improve outcomes for patients with inherited renal tubulopathies. Full article

Nephrolithiasis is a prevalent urological disorder worldwide, whose pathogenesis involves a complex network of crystal formation, cellular injury, and microenvironmental dysregulation. As a critical mechanism for regulating cellular functions, protein post-translational modifications (PTMs) have been increasingly implicated in multiple facets of kidney stone formation, including crystal–cell interactions, oxidative stress responses, and inflammatory signaling pathways. This review systematically synthesizes the biochemical foundations of PTMs, the molecular microenvironment of nephrolithiasis, and the roles of key modifications such as phosphorylation and acetylation in the pathogenesis of calculi. It further explores the translational potential of PTM detection technologies in clinical practice. Current evidence indicates that PTMs influence the nucleation, growth, and aggregation of crystals by modulating the activity of pro-/anti-lithogenic proteins, the expression of cell adhesion molecules, and inflammatory pathways. Consequently, therapeutic strategies targeting PTMs may offer novel avenues for the prevention and management of kidney stones. Future research should focus on integrating multi-omics approaches with functional validation to elucidate the dynamic regulatory networks of PTMs within the stone microenvironment, thereby advancing the development of precision medicine. Full article

Background: Nephrolithiasis is a significant global health and economic challenge, with an increasing prevalence and a high recurrence rate. However, there is limited knowledge regarding the potential associations between calcium nephrolithiasis risk and Chinese Han populations currently. Methods: To identify the genetic factors for calcium nephrolithiasis, we presented a genome-wide association study (GWAS) using a total of 1006 calcium nephrolithiasis cases and 1200 controls of Chinese Han ethnicity. Suggestive loci (p < 1.0 × 10⁻⁶) were replicated in 445 cases and 1008 controls. We also assessed the association of GWAS-level significant single-nucleotide polymorphisms (SNPs) with quantitative traits, including metabolic, kidney-related, and electrolyte traits. Results: Here we found three novel loci for calcium nephrolithiasis: SORBS2 on 4q35.1 (rs3736194; p = 2.84 × 10⁻¹³, OR = 0.6279), CXXC5 on 5q31.2 (rs356450; p = 6.09 × 10⁻¹⁶, OR = 2.0312), and MBD2 on 18q21.21 (rs55826947; p = 6.29 × 10⁻¹⁰, OR = 0.6017). Subsequent analyses revealed the association of SNP rs3736194 with higher serum carbon dioxide (p = 0.04666), rs356450 with lower serum chloride (p = 0.02992), and rs55826947 with higher BMI (p = 0.03174), respectively. Conclusions: We performed the first GWAS on calcium nephrolithiasis in a Chinese Han population cohort and identified three novel susceptibility loci on 4q35.1, 5q31.2, and 18q21.2. Further research into the molecular mechanisms underlying these variations in nephrolithiasis is warranted. Full article

Background and Objectives: Because of its consistently high stone-free rates (SFRs), percutaneous nephrolithotomy (PCNL) continues to be the first-line treatment for renal stones larger than 20 mm. Standard 24 to 30 Fr access tracts, however, are linked to access-related morbidity, such as bleeding, pain, and extended hospital stays. These restrictions have led to progressive tract miniaturization and the development of mini-PCNL, ultra-mini PCNL, and micro-PCN techniques. Materials and Methods: We performed a narrative review of studies published through January 2026 using PubMed and Google Scholar. Search terms included percutaneous nephrolithotomy, mini-PCNL, ultra-mini PCNL, micro-PCNL, and vacuum-assisted PCNL. Original studies, systematic reviews, and meta-analyses reporting clinical outcomes, complications, and advancements were selected, whereas conference abstracts, non-English papers, and articles without accessible full text were excluded. Results: Across randomized trials, miniaturized PCNL generally preserves efficacy when patients are selected appropriately. Across randomized trials and meta-analyses, miniaturized PCNL achieved stone-free rates comparable to standard PCNL (typically ~80–90% for stones ≤20 mm and similar rates in selected stones >2 cm), while demonstrating lower hemoglobin decrease (mean difference approximately −0.6 to −1.0 g/dL), reduced transfusion rates, and shorter hospital stays, at the cost of longer operative time (mean difference ~8–12 min). On the other hand, operative time may increase, and smaller working channels can make visualization and fragment evacuation more demanding as stone burden rises. Raised intrarenal pressure is a recurring safety issue because it may increase infectious risk unless drainage is actively managed. Recent innovations aim to address these limitations, including vacuum-assisted access sheaths, pressure-controlled irrigation, improved laser and lithotripsy platforms, image-fusion guidance, navigation systems, and robotic assistance. Conclusions: PCNL now spans a spectrum of tract sizes rather than a single standard approach. When chosen appropriately and performed with attention to pressure control and fragment evacuation, miniaturized PCNL can reduce morbidity without sacrificing stone clearance. Future advancements in percutaneous stone surgery are more likely to rely on integrated technological solutions that improve accuracy, safety, and repeatability than on additional tract size reduction. Full article

Introduction: Vitamin D deficiency [25(OH)D < 30 ng/mL] is widely prevalent globally and the efforts to tackle it have been rather unsuccessful to date. Despite different cutoffs used to define it, many clinicians adhere to the 2011 Endocrine Society definition. We present a special treat-to-target protocol aiming to restore and maintain vitamin D sufficiency. Methods: We reviewed the efficacy and safety of our vitamin D supplementation protocol over 5 years, and compared it to a group of patients who self-reported never taking vitamin D supplements. We recorded the baseline, 2-month, and annual 25(OH)D (D) measurements, along with subjects’ age, sex, BMI, history of osteoporosis, nephrolithiasis, nephrocalcinosis, and renal colics. According to our supplementation protocol, replenishment of vitamin D involves cholecalciferol dosing in two steps: a loading dose (LD) for 2 months and a maintenance dose (MD) thereafter. Please refer to the main text for loading and maintenance dose titration. Results: Of 8329 cases with vitamin D measurements, 2248 had adequate follow up data of 3524.5 patient-years and were included in the study: a total of 1575 intervention subjects and 673 controls, with an average follow-up of 18.8 months. Baseline vitamin D concentrations of 22.6 ng/mL (controls) did not change significantly (2 months: 22.2; 1 year: 21.7; 2 years: 22.0; 3 years: 23.8; 4 years: 21.8; and 5 years: 22.1 ng/mL), while concentrations of 21.9 ng/mL (intervention group) reached and remained 40 ng/mL (2 months: 41.0; 1 year: 39.4; 2 years: 39.0; 3 years: 39.3; 4 years: 40.4; and 5 years: 39.4 ng/mL). Vitamin D adequacy was achieved in 91.6% of patients in the intervention arm compared to only 16.9% in controls (p < 0.0001). Mean D and rates of adequacy were significantly higher over time in the intervention arm (p < 0.0001). The incidence of renal adverse events or hypervitaminosis did not differ between groups (p > 0.05). Conclusions: Our intervention protocol appears highly efficient in achieving and maintaining vitamin D adequacy over 5 years, with no increase in adverse events compared with controls, presenting it as an effective long-term strategy. Full article

Primary hyperoxalurias (PHs) are rare autosomal recessive disorders characterized by overproduction of oxalate, a metabolic end product that readily forms calcium oxalate crystals. Excess hepatic oxalate leads to recurrent kidney stones, nephrocalcinosis, and progressive renal injury, often culminating in end-stage kidney disease (ESKD). Once renal clearance declines, systemic oxalate accumulation can cause multisystem deposition. PH encompasses three types—PH1, PH2, and PH3—caused by deficiencies in the hepatic enzymes AGT, GRHPR, and HOGA1, respectively, resulting in accumulation of glyoxylate and subsequent oxalate overproduction. Clinical presentation varies from infantile oxalosis to adult-onset recurrent nephrolithiasis, with PH1 generally being the most severe. Diagnosis relies on urinary oxalate measurements, plasma oxalate in advanced chronic kidney disease, urinary metabolite profiling, imaging, and genetic testing. Management includes hyperhydration, citrate supplementation, pyridoxine for responsive PH1 patients, dialysis and transplantation when required, while RNA interference therapies targeting glycolate oxidase or LDHA have demonstrated substantial biochemical efficacy in PH1 and represent promising emerging therapeutic options, although long-term clinical outcome data remain limited and broader applicability to other PH types is still under investigation. Future strategies focus on modulating intestinal oxalate absorption, gut microbiome therapies, oxalate-degrading enzymes, and novel gene-editing approaches. Early diagnosis and individualized management are critical to prevent kidney injury and systemic oxalosis. In this review, we summarize the genetic, biochemical, and clinical features of PH and discuss current and emerging therapeutic strategies. Full article