Omissions in clinical documentation hinder diagnosis by obscuring important information and delaying communication among clinicians. Additionally, carefully implemented incentives can improve health care processes such as clinical documentation. Therefore, we created a pilot using $20,000 in compensation incentives to improve free text documentation for six common outpatient diagnoses (cerebrovascular accidents, chronic kidney disease, congestive heart failure, deep vein thrombosis and pulmonary embolism, chronic obstructive pulmonary disease, and smoking) in an urban health system. For each diagnosis, we asked clinicians to document 2-3pre-specified clinically significant, evidence-based details that influence diagnosis or management. We compared baseline documentation (Aug 15th-Sep 25th, 2022) with an incentivized period (Sep 26th-Dec 16th, 2022) using an unadjusted signed rank test and an adjusted generalized linear mixed model. All 32 eligible physicians and advanced practice providers participated. Among 693 baseline and 1,494 intervention opportunities when a diagnosis was assessed, documentation that included all clinically significant details improved from mean 32.2 % (SD 20.7) to mean 47.1 % (SD 23.6; p=0.01) and in our adjusted analysis from 35.6 to 48.2 % (p<0.001). Seven participants' documentation improved by≥1.6 diagnoses perweek. In conclusion, compensation incentives improved free text documentation of clinically significant information to improve the diagnostic process.

Chronic kidney disease (CKD) is pathologically characterized by oxidative stress, inflammation, and renal fibrosis, yet effective therapeutic interventions for this condition remains limited. Grifola frondosa polysaccharide (GFP), an active component derived from the edible and medicinal mushroom G. frondosa, has demonstrated antioxidant, anti-inflammatory, and anti-tumor properties. However, its renoprotective effects against CKD and the underlying molecular mechanisms have not been thoroughly elucidated. Structural analysis revealed that GFP contained pyranose rings with both α- and β-glycosidic linkages. In the adenine-induced CKD mouse model, GFP administration significantly alleviated renal dysfunction and pathological damage, as evidenced by improvements in body weights, kidney index, serum biochemical parameters, and histological findings. Furthermore, GFP administration enhanced renal antioxidant capacities while reducing malondialdehyde contents. GFP also suppressed systemic and renal inflammatory responses, as evidenced by decreased levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Importantly, GFP treatment suppressed renal fibrosis by down-regulation of kidney injury molecule-1 (Kim-1) and transforming growth factor-β1 (TGF-β1) expressions, as well as modulation of the TGF-β1/Smad signaling pathway. Our findings demonstrated that GFP exerted potent renoprotection against adenine-induced CKD in mice, mediated by its antioxidant, anti-inflammatory, and anti-fibrotic activities. The anti-fibrotic mechanism was mediated via the suppression of the TGF-β1/Smad signaling pathway. These results highlighted the potential of GFP as functional food ingredients or adjunctive therapeutic agents for preventing and treating CKD and its complications. © 2026 Society of Chemical Industry.

BackgroundThe nonsteroidal mineralocorticoid receptor antagonist finerenone has been reported to improve kidney and cardiovascular outcomes in persons with type 2 diabetes and chronic kidney disease (CKD). The efficacy and safety of finerenone in persons with type 1 diabetes and CKD are unknown.MethodsWe conducted a phase 3 trial involving adults who had type 1 diabetes, CKD (estimated glomerular filtration rate [eGFR], 25 to <90 ml per minute per 1.73 m2 of body-surface area), and albuminuria (urinary albumin-to-creatinine ratio [with albumin measured in milligrams and creatinine measured in grams], 200 to <5000) and were receiving an angiotensin-converting–enzyme (ACE) inhibitor or an angiotensin-receptor blocker. Participants were randomly assigned to receive finerenone (10 or 20 mg per day, depending on the eGFR) or matching placebo. The primary outcome was the relative change in the urinary albumin-to-creatinine ratio over a period of 6 months.ResultsA total of 242 participants underwent randomization. The median urinary albumin-to-creatinine ratio decreased from 574.6 at baseline to 373.5 at 6 months among all the participants assigned to receive finerenone and from 506.4 to 475.6 among those assigned to receive placebo. Over a period of 6 months, the urinary albumin-to-creatinine ratio decreased by 34% with finerenone (geometric mean ratio to baseline, 0.66; 95% confidence interval [CI], 0.60 to 0.73) and 12% with placebo (geometric mean ratio to baseline, 0.88; 95% CI, 0.79 to 0.98), which corresponded to a 25% greater reduction with finerenone than with placebo (geometric mean ratio for finerenone vs. placebo, 0.75; 95% CI, 0.65 to 0.87; P<0.001). The most common adverse event was hyperkalemia (in 12 participants [10.1%] with finerenone and in 4 [3.3%] with placebo); 2 participants (1.7%) discontinued finerenone because of hyperkalemia. At 6 months, the change in the eGFR was –5.6 ml per minute per 1.73 m2 with finerenone and –2.7 ml per minute per 1.73 m2 with placebo (difference, –2.9 ml per minute per 1.73 m2; 95% CI, –5.1 to –0.7); eGFR values approached baseline levels during the washout period.ConclusionsIn adults with type 1 diabetes and CKD, finerenone resulted in a significantly greater decrease in the urinary albumin-to-creatinine ratio than placebo. (Funded by Bayer; FINE-ONE ClinicalTrials.gov number, NCT05901831.)

Ten-Year Clinical Outcomes and Cause of Death in Patients on Dialysis Undergoing Percutaneous Coronary Intervention: A Retrospective Mayo Clinic PCI Registry Analysis.

Diabetic patients undergoing percutaneous coronary intervention (PCI) frequently have complex coronary artery disease (CAD) and suboptimal outcomes with drug-eluting stents (DES). Sirolimus-coated balloons (SCB) have recently been introduced, but comparative data versus DES in diabetic patients with de novo CAD are lacking. The SIMPLE-DM study is a pooled analysis of five observational registries including all-comer diabetic patients undergoing PCI for de novo CAD. Patients in the SCB cohort were treated with the phospholipid nanocarrier Magic Touch SCB, while those in the DES cohort received current-generation DES. Propensity score (PS) adjustment was used to balance clinical and angiographic characteristics. The primary endpoint was the 2-year cumulative incidence of target lesion failure (TLF), defined as the composite of cardiac death, target vessel MI (TV-MI), or target lesion revascularization (TLR). A total of 1838 patients were included, 599 treated with SCB-based PCI and 1239 with DES-only PCI. At 2 years, TLF occurred in 9.1% of SCB and 9.9% of DES patients (adj. hazard ratio HR 0.88, 95% confidence interval CI 0.43-1.81, p = 0.736). No significant differences were found in cardiac death, TV-MI or TLR. SCB-based PCI was associated with more favourable outcomes in patients with chronic kidney disease (p for interaction = 0.042) and long lesions (p for interaction = 0.003), whereas DES-only PCI performed better in those with short lesions. In diabetic patients undergoing PCI for de novo CAD, an SCB-based strategy was associated with comparable 2-year outcomes to DES-only PCI, with signals of potential benefit in the highest clinical and anatomical risk subsets.

The ability to predict the three-dimensional structure of a protein from its amino acid sequence has potential to provide insights into its function, and in the context of disease, its pathogenic mechanisms and potential drug targets. Artificial intelligence (AI)-driven algorithms, particularly AlphaFold and RoseTTAFold, have revolutionized the field of protein modelling, enabling rapid, high-confidence predictions of protein structures. In nephrology, these advances have clarified the molecular architecture of key renal systems such as podocyte slit diaphragm complexes, the conformational states of membrane transporters and the structural basis of channelopathies that affect polycystin channels. These developments have also enabled low-resolution modelling of complex macromolecular structures, providing insights into structural changes that might underlie the pathogenesis of disease mutants, and enabled virtual screening of drugs and toxins. Although these AI models have yielded important new insights, their integration with experimental methods, particularly cellular cryogenic electron tomography, remains crucial for capturing the domain flexibility, conformational dynamics and binding specificity of proteins in their native environment. Combining AI-based structure prediction with experimental validation will uncover novel pathophysiological mechanisms, guide drug discovery and reveal potential new avenues to target mechanisms of kidney disease.

Vitamin D, a fat-soluble vitamin functioning as a hormone via the vitamin D receptor (VDR), is critical for calcium homeostasis and bone health. Vitamin D deficiency is linked to nutritional rickets, osteomalacia, and increased risk of non-communicable diseases such as cancer and diabetes. While serum 25(OH)D3 is used to assess vitamin D status, its active form, 1α,25(OH)2D3, exerts context-dependent effects on calcium metabolism. Nonetheless, the therapeutic utility of native vitamin D is limited in certain pathologies. In chronic kidney disease (CKD), the renal conversion of 25(OH)D3 to active 1α,25(OH)2D3 is compromised, necessitating the use of active synthetic analogs to bypass this metabolic defect. Furthermore, for dermatological and oncological disorders requiring supraphysiological dosing, synthetic analogs have been designed to dissociate beneficial anti-proliferative effects from the severe hypercalcemia induced by high-dose 1α,25(OH)2D3. VDR mediates transcriptional responses, modulated by co-regulators and chromatin remodeling complexes. Recent discoveries include non-genomic VDR pathways and SCAP (SREBP cleavage-activating protein)-dependent signaling that modulate lipid metabolism. Despite promising preclinical results, most synthetic VDR agonists fail to show efficacy in cancer therapy due to calcemic toxicity. However, compounds like eldecalcitol are effective in osteoporosis, especially in low-calcium-intake populations. Selective VDR modulators, akin to SERMs, exhibit tissue-specific effects. Moreover, novel VDR antagonists such as ZK168281 demonstrate potential to suppress hypercalcemia and vitamin D toxicity by inhibiting transcriptional activity and altering VDR localization. These agents may enable anti-inflammatory or anti-proliferative actions without calcemic risks. Understanding the nuanced biology of vitamin D and its analogs offers new avenues for therapeutic intervention beyond bone metabolism, including managing hyperparathyroidism, granulomatous diseases, and inflammation-associated disorders.

Indoxyl sulfate (IS), one of protein bound uremic toxins, is associated with various complications in chronic kidney disease patients and could partially be removed through hemodialysis and hemoperfusion due to its high affinity to human serum albumin. Many studies have demonstrated the potential for blood purification applications, such as poly-β-cyclodextrin (PCD) and metal-organic frameworks, providing new possibilities for the efficient removal of IS. Here, we utilizedβ-cyclodextrin (β-CD)-grafted polyethyleneimine (PEI), which is referred to asβP, as a scavenger for IS and sodium alginate (SA) as the matrix material to prepare alginate-based hybrid macrospheres (MS). The surface polydopamine (PD) and argatroban (AG) modification resulted in enhanced biocompatibility and anticoagulation. The results indicated that the hybrid MS demonstrated effective adsorption and removal capacity (79.96%) of IS. Moreover, the lower hemolysis rate (0.36%) and longer anticoagulation-related factors (APTT: 161.5 s; TT, 35.6 s) also revealed favorable biocompatibility and anticoagulation. This study presents a new way to designate blood purification materials and highlights their potential in clinical hemoperfusion treatment.

Almost 10% of the global population suffers from chronic kidney disease (CKD). The inexistence of a therapeutic to restore renal function motivates the scientific community to search for new treatments. The 5/6 nephrectomy (Nx) rat model is widely used to mimic human CKD, but the impact of strain-specific responses on disease progression remains unclear. Here, we aimed to compare CKD development in Wistar, Lewis, and Fischer rats submitted to the Nx model. In summary, even submitted to the same surgical procedure, the three studied rat strains presented distinct patterns of CKD progression: Wistar rats exhibited faster and sustained renal function loss, with exuberant hypertension, proteinuria, and renal inflammation, being considered as excellent models to study rapidly progressive human nephropathy. Lewis animals, in turn, presented mild low-progressive CKD, which make this rat strain especially useful to simulate intermediate degrees of human CKD and to develop long-term tests. Finally, Fischer rats submitted to Nx did not even develop hypertension, proteinuria, or glomerular damage within 30 days. Moreover, compared to Wistar rats, both Lewis and Fischer animals have a relatively higher basal number of nephrons and a lower number of whole blood leukocytes, which may have contributed to the renoprotection exhibited by these rat strains.

Integrated lifestyle management to mitigate MASLD risk in patients with chronic kidney disease: a prospective cohort study.

Cardio-kidney-metabolic (CKM) syndrome combines cardiac, renal, and metabolic impairments. Albuminuria, as measured by the urine albumin-to-creatinine ratio, is a biomarker of endothelium-glomerular damage present in CKM syndrome. The gold standard method is quantitative measurement using an immunoenzymatic technique in a laboratory. Albuminuria is continuously associated with cardiovascular risk, even when the increase is modest. The improvement in cardiovascular prognosis achieved with treatments that reduce albuminuria suggests that CKM syndrome is reversible through multiple mechanisms. It is recommended measuring albuminuria in patients with arterial hypertension, chronic kidney disease, or diabetes, and then identifying those who may benefit from cardioprotective treatment.

Factors associated with employment in end-stage kidney disease patients at the initiation of chronic dialysis or kidney transplantation-a national register-based cohort study.

Cardiovascular-kidney-metabolic (CKM) disease and chronic obstructive pulmonary disease (COPD) are associated with major adverse cardiovascular events (MACE). Whether COPD further increases MACE risk within CKM populations, and whether this potential risk is modifiable through inhaled corticosteroids (ICS), is unknown. Within CKM populations, we investigated the relationship between (1) COPD and subsequent MACE, and (2) amongst concurrent CKM-COPD populations, we investigated the relationship between ICS and subsequent MACE. We used Clinical Practice Research Datalink (CPRD) Aurum, Hospital Episode Statistics and Office of National Statistics data, between January 1st, 2010, and March 29th, 2021. We created five discrete cohorts: chronic kidney disease (CKD), type-II diabetes mellitus (T2DM), obesity, MACE history, and older adults (aged ≥ 65years old ["Age65 + "]). CKD, T2DM, obesity, and Age65 + cohorts were MACE-naïve at the time of inclusion. Aim (1) exposures were (a) COPD, (b) incident COPD, and (c) being at risk of COPD without diagnosis (defined as age ≥ 40years old, smoking history, no evidence of asthma, and frequent respiratory infections requiring antibiotics). Aim (2) exposure was ICS prescription (control group: long-acting bronchodilators). The outcome was MACE (acute coronary syndrome, arrhythmia, heart failure, ischaemic stroke, or cardiovascular-specific mortality). We implemented Cox proportional hazards models. COPD was associated with MACE amongst all cohorts, but was comparatively weak in the MACE history cohort (cohort total; adjusted hazard ratio [95% confidence interval]): CKD (N = 573,626; 1.29 [1.26, 1.32]), T2DM (N = 649,506; 1.30 [1.26, 1.35], obesity (N = 225,273; 1.41 [1.34, 1.48]), MACE history (N = 507,889; 1.04 [1.02, 1.06]), and Age65 + (N = 592,123, 1.59 [1.52, 1.66]). Incident COPD was associated with subsequent MACE in CKD only (1.28 [1.13, 1.45]). Being at risk of COPD was associated with subsequent MACE in CKD (1.18 [1.07, 1.30]), MACE history (1.16 [1.08, 1.25]), and Age65 + (1.28 [1.13, 1.46]). ICS prescription was not associated with subsequent MACE in any concurrent CKM-COPD cohort. COPD was an independent risk factor for MACE in CKM populations. ICS did not attenuate MACE amongst CKM-COPD groups. Incident COPD was associated with MACE in CKD, and being at risk of COPD was associated with MACE in CKD, MACE history, and Age65 + cohorts.

Accurate, noninvasive assessment of renal fibrosis (RF) in chronic kidney disease (CKD) remains challenging. This study aimed to develop and externally validate a dual-center multi-sequence MRI radiomics nomogram integrating imaging and clinical parameters for evaluating RF severity. This retrospective dual-center study included 164 patients with CKD who underwent multi-sequence MRI and renal biopsy, divided into a training set (n = 128) and an external test set (n = 36). Radiomics features were extracted from intravoxel incoherent motion (IVIM) and blood oxygenation level-dependent (BOLD) MRI. Feature selection involved inter-observer correlation coefficient, Mann-Whitney U test, Pearson correlation coefficients, and least absolute shrinkage and selection operator regression. Three radiomics models (Rad_IVIM, Rad_BOLD, Rad_IVIM+BOLD) and one clinic model were developed to distinguish mild from moderate-to-severe RF. A nomogram was constructed by integrating the Rad_IVIM+BOLD score with significant clinical variables. Model performance was evaluated using area under the curve (AUC), DeLong test, decision curve analysis (DCA), and calibration curves. The Rad_IVIM+BOLD model achieved AUCs of 0.898 (95% confidence intervals [CI]: 0.845-0.951) in the training set and 0.749 (95% CI: 0.584-0.914) in the test sets, showing a favorable performance trend compared with the single-sequence radiomics models. The nomogram demonstrated good discrimination with AUCs of 0.922 (95% CI: 0.876-0.969) and 0.861 (95% CI: 0.728-0.993) in the training and test sets, respectively. The DeLong test showed its superiority over the clinic and radiomics models. DCA and calibration curves further confirmed its high predictive value and robustness. A nomogram combining multi-sequence MRI radiomics and clinical features provides a noninvasive tool for assessing RF severity in CKD, supporting quantitative imaging-guided clinical decision-making and disease follow-up.

Black individuals bear a disproportionate burden of kidney diseases, including genetically mediated risk related to Apolipoprotein L1 (APOL1) gene variants. Awareness of APOL1-mediated kidney disease (AMKD) and participation in therapeutic trials remain low. Whether different engagement strategies can raise awareness and identify trial-eligible individuals is uncertain. The Community APOL1 Research Engagement (CARE) study aimed to increase AMKD awareness through culturally tailored education and screening while building a clinical trial-eligible registry, CARE registry, to support a phase 2 baricitinib trial for AMKD in the Janus kinase-STAT Inhibition to Reduce APOL1-Associated Kidney Disease (JUSTICE). The CARE study was conducted from May 2022 through July 2025 across community and clinical settings in multiple U.S. regions, in partnership with churches with predominantly Black attendees. Black adults aged 18-70 years without diabetes or dialysis dependence underwent APOL1 genotyping and kidney disease screening. Recruitment occurred via community events, electronic health record (EHR) queries, physician referrals, and self-referrals. The primary outcome was eligibility for the CARE Registry, defined by APOL1 high-risk genotype, urine-albumin-to-creatinine ratio (UACR) ≥300 mg/g and eGFR ≥25 mL/min/1.73 m2. Of 1,052 individuals approached, 789 (75%) consented to screening. Overall, 128 (17%) carried APOL1 high-risk genotypes. Community events accounted for most enrollments (83%) but yielded low rates of registry-eligible albuminuria (1%). In contrast, EHR queries and physician referrals identified higher proportions of participants with APOL1 high-risk genotypes and UACR ≥300 mg/g. Twenty-four participants met CARE Registry criteria, and seven enrolled in the JUSTICE trial. Refusal was 4% and attrition was 2%. Community engagement achieved high participation and awareness but was less efficient for identifying trial-eligible individuals than EHR- and provider-based approaches.

Kidney Disease: Improving Global Outcomes (KDIGO): navigating a rapidly changing landscape.

Apoptotic bodies are membrane-bound vesicles generated during the terminal stages of programmed cell death and traditionally viewed as inert cellular debris. Emerging evidence, however, positions apoptotic bodies as dynamic mediators of intercellular communication with critical roles in renal physiology and pathology. In the healthy kidney, efficient efferocytosis of apoptotic bodies maintains tissue homeostasis by ensuring immunologically silent clearance of apoptotic remnants. In acute kidney injury (AKI), extensive tubular epithelial apoptosis generates a high burden of apoptotic bodies that can amplify inflammation, endothelial dysfunction, and adaptive immune activation when clearance is impaired, yet promote resolution and epithelial repair when efficiently removed. In chronic kidney disease (CKD), persistent low-grade apoptosis combined with defective efferocytosis leads to progressive accumulation of apoptotic bodies in the interstitium, where their bioactive cargo-including DAMPs, cytokines, growth factors, and profibrotic microRNAs-drives fibroblast activation, extracellular matrix expansion, and fibrosis. In the vasculature, apoptotic bodies derived from vascular smooth muscle cells act as nucleation sites for calcium-phosphate crystal deposition, linking apoptosis to the development of medial vascular calcification in CKD. Together, these findings highlight apoptotic bodies as active regulators of injury, inflammation, fibrosis, regeneration, and vascular pathology. Understanding the determinants of their pathogenic versus reparative effects could yield new biomarkers and therapeutic strategies, including modulation of efferocytosis, targeting apoptotic body-derived signaling pathways, and engineering apoptotic bodies-based delivery systems.

Background: Glomerular disease (GD) and diabetic nephropathy are both leading causes of end-stage kidney disease (ESKD) in the United States. Much is known about each individually, but less of any interactions between the two. There is emerging evidence that factors specific to glomerular disease, such as immunosuppression, may increase the risk of diabetes, which in turn could compound glomerular filtration rate (GFR) decline through the mechanisms of diabetic nephropathy. Understanding the epidemiology of prediabetes and diabetes in glomerular disease patients may inform improved screening and prevention practices in this population and may lead to strategies that mitigate progression to ESKD. The aim of this study is to delineate risk factors for prediabetes in glomerular disease. Methods: Data was extracted from University of Michigan and Kidney Research Network electronic health record registry with patients classified by age at glomerular disease at diagnosis or first nephrology appointment (child (age&lt;18y, n=406) and adult (≥ 18y, n=339)). A Cox proportional hazards model was calculated using prediabetes after kidney disease onset as the outcome, adjusted for age, sex, race, weight, hypertension, and defined relevant drug prescriptions. A subgroup analysis was performed to track the progression from prediabetes to diabetes. Results: 148 patients (19.9% of cohort) developed prediabetes in study follow-up. Adult GD patients were more likely than pediatric GD patients to progress (HR: 1.73 [95%CI: 1.19 - 2.50]), as were patients with uncontrolled hypertension (HR: 9.61 [95%CI: 3.02 - 30.61]) and controlled hypertension (HR: 6.50 [95%CI: 1.91 - 22.18]). The use of beta blockers, statins, or diuretics was also associated with higher prediabetes risk (HR: 2.87 [95%CI: 1.98 - 4.17]). Conclusions: Adult age, worsening control of hypertension, and certain medications were associated with increased prediabetes risk in pre-existing glomerular disease. More data, in particular prospective data, is needed to refine risk relationships and incidence data.

Chronic diseases—including diabetes mellitus, cardiovascular disease, chronic kidney disease, and autoimmune disorders—remain the leading causes of global morbidity and mortality. While biomedical pathophysiology defines the etiology and progression of these conditions, cultural factors significantly modulate how patients perceive illness, engage in treatment, and adhere to medical recommendations. This review synthesizes evidence from cross-cultural studies, with a specific focus on medical manifestations and therapeutic challenges, to examine how sociocultural determinants intersect with biological disease processes. We highlight nuanced case comparisons between South Asian, East Asian, Middle Eastern, African, Latinx, and Indigenous populations, illustrating how cultural constructs such as collectivism, fatalism, stigma, reliance on traditional medicine, and health literacy directly influence outcomes in chronic disease management. Importantly, we integrate evidence-based recommendations for healthcare professionals, emphasizing culturally tailored interventions, precision medicine approaches, and the role of interdisciplinary care teams.

Objective. To identify predictors of poor prognosis in patients with arterial hypertension (AH) without associated clinical conditions who have long-term post-COVID syndrome (LPS). Materials and methods. This work presents a subanalysis of a prospective observational study, which included 258 patients with AH and LPS according to the inclusion and exclusion criteria. The incidence of fatal events and any hospitalizations was recorded throughout the follow-up period. At the end of the follow-up period, the patients were divided into 2 groups based on prognostic parameters: Group 1 included 65 patients who experienced adverse events, and Group 2 comprised 193 patients with no fatal events and hospitalizations during the observation period. Results. In 33.7 % of patients with uncomplicated AH, the development of LPS was associated with a risk of all-cause mortality (4.6 %) and hospitalizations (95.4 %) after 22.5 ± 8.4 months of follow-up. Uncontrolled AH based on home measurement, failure to achieve the target nocturnal blood pressure (BP), and a morning systolic BP surge 56 mm Hg increased the relative risk (RR) of an adverse prognosis in patients with AH, LPS, and no associated clinical conditions by 1.9-fold; a non-dipper/night-peaker circadian BP profile increased it by 3.2-fold; a mean 24-hour pulse pressure 53 mm Hg increased it by 2-fold; and nocturnal masked AH increased it by 3.6-fold. Structural and functional left ventricular (LV) remodeling characterized by LV diastolic dysfunction, LV hypertrophy, elevated N-terminal pro-brain natriuretic peptide (NT-proBNP) levels, and indicative of preclinical chronic heart failure (CHF) in patients with uncomplicated AH and LPS without symptoms and signs of circulatory insufficiency, increased the RR of an adverse prognosis by an average of 2–2.5 times. Only an estimated glomerular filtration rate (eGFR) 60 ml/min/1.73 m2 (calculated using cystatin C alone or its combination with creatinine), and a urinary protein-to-creatinine ratio 300 mg/g, indicated a poor prognosis in patients with uncomplicated AH and LPS, increasing the RR by 2.0, 1.2, and 1.8 times, respectively. The development or progression of chronic kidney disease (CKD) in patients with AH and LPS increased the RR of poor prognosis by 2.2-fold. Conclusions. LPS in patients with uncomplicated AH is associated with a high incidence of adverse prognosis. The predictive value for adverse outcomes in this patient population was demonstrated by indicators reflecting the uncontrolled course of AH, particularly at night and early in the morning, the presence of preclinical CHF and CKD.