Helicobacter pylori (H. pylori) is a common gastric pathogen that is linked to peptic ulcers, gastric cancer and systemic disorders. There is emerging evidence of an association between infection with H. pylori and chronic kidney disease and non-alcoholic hepatic steatosis, and possible renal and hepatic involvement. This study was conducted to assess the relationship between H. pylori and kidney and liver function changes in Saudi Arabian people. Blood samples were collected from 82 participants divided into two groups, namely H. pylori-infected and non-infected. Biochemical analyses were done to determine kidney (creatinine, urea, sodium and potassium) and liver function (ALT, AST, ALP, total protein and albumin). A total of 82 participants were included in the study, of whom 42 (51.2%) tested positive for Helicobacter pylori infection, while 40 (48.8%) were non-infected and served as the control group. Liver enzyme levels (ALP (64.00), AST (21.40), ALT (21.26) and GGT (20.78)) were normal and did not differ significantly between groups (p > 0.05). Regression analysis showed a significant relationship between H. pylori infection and high creatinine (OR = 6.38, p = 0.018). Borderline correlations were found for GGT (OR = 1.179, p = 0.092), uric acid (OR = 2.661, p = 0.061), and the electrolytes and lipid profiles showed no significant variation. H. pylori infection was significantly related to elevated creatinine levels, and may be affecting renal function. Most liver and electrolyte parameters were not affected. Further studies with larger cohorts are required in order to confirm these findings.

Introduction: chronic inflammation and malnutrition have play a fundamental roles in muscle loss. Albumin, globulin and albumin globulin ratio (AGR) are considered as useful ideal biomarker of inflammation and nutritional status. A lot of studies reveal the relationship of this biomarkers with muscle loss in adult but there is no studies demonstrate obviously this relation in young people so this study was aimed to investigate to detect the prevalence of sarcopenia (low muscle mass) and relationship of it with albumin level, total protein level, globulin level and AGR in student young population. Subjects and methods: this study was carried out in the department of medical laboratory science of Jazan University from September 2025 to December 2025 in Jazan University. A hundred apparently healthy male and female medical students between ages of 18-30 years were recruited in this study based on a defined inclusion and exclusion criteria. A questionnaire form with detail of sex, age, weight, height was obtained. Approximately 5 ml of venous blood was collected for measurement of total protein level and albumin level. Globulin was calculated by subtracting total protein level from albumin level. AGR was calculating by dividing albumin and globulin. Appendicular skeletal mass index (ASMI) was estimated using the following validated equation: ASM = 0.193 × body weight + 0.107 × height − 4.157 × gender − 0.037 × age − 2.631 (Weight in kg; height in m; age in years; gender: 1, for men and 2, for women) with cutoff less than 7.3 in male and less than 5.0 in female. Result: Scatter diagram and Pearson correlation was used to determine the relation of skeletal mass (ASMI) with albumin, total protein, globulin and AGR in male and female medical students. 29% of total male student with sarcopenia while 16% is the prevalence of sarcopenia among female student. In male students: albumin, total protein and AGR was positively correlate with muscle mass while globulin was show no correlation. In female students: total protein and globulin were positively correlate while AGR was negatively correlate with muscle mass and albumin was show no any statistical correlation. Conclusion: the relationship between albumin, globulin albumin to globulin ratio and muscle mass were depend on sex (sex-specific).

Background: COVID-19-associated acute kidney injury (AKI) is common in severe disease, but its long-term kidney implications are heterogeneous and incompletely defined. Objective: To synthesize recovery phenotypes and longitudinal outcomes, reconcile conflicting evidence on whether COVID-associated AKI differs from other-cause AKI, and set out implications for surveillance and management. Methods: The evidence base was assembled through a targeted PubMed/MEDLINE search for COVID-19 and kidney dysfunction (January 2020 to August 2026), hand-searching of reference lists, and direct retrieval of pivotal longitudinal cohorts and clinical practice guidelines. Longitudinal cohorts and comparative studies were prioritized. Findings: AKI severity, duration, kidney replacement therapy, lower baseline estimated glomerular filtration rate (eGFR), and incomplete early recovery consistently identify patients at greatest risk. Longitudinal studies disagree on whether COVID-AKI confers more risk than AKI from other illnesses: early cohorts reported steeper eGFR loss, whereas a later 9624-patient cohort found lower adjusted major adverse kidney events. This divergence reflects differences in kidney reference point, outcome construction, ascertainment, and handling of competing death rather than genuine contradiction. Population studies show long-term kidney failure is concentrated after hospitalization and severe disease. Candidate biomarkers remain investigational. Conclusions: Post-COVID kidney risk is severity- and phenotype-dependent rather than universal. Follow-up is most defensible after hospitalized AKI, incomplete recovery, advanced chronic kidney disease (CKD), dialysis, or transplantation and applies existing post-AKI guidance rather than a COVID-specific schedule. Survivors who meet Kidney Disease: Improving Global Outcomes (KDIGO) criteria for CKD at three months, namely a GFR below 60 mL/min/1.73 m² or a persistent marker of kidney damage, become eligible for guideline-directed therapy, though no trial has enrolled on recent AKI. Prospective studies should test whether structured follow-up improves outcomes.

Background and Objectives: Thyroid dysfunction and dysglycemia often coexist, but cross-sectional associations may reflect the populations sampled rather than a graded biochemical relationship. We compared the glycemic profile of adults with abnormal thyroid function tests with that of a euthyroid comparison group and examined whether thyrotropin (TSH), free thyroxine (FT4) and free triiodothyronine (FT3) were associated with glycated hemoglobin (HbA1c) and fasting plasma glucose (FPG) within groups. Materials and Methods: This cross-sectional study included 331 adults from Jazan, Saudi Arabia: 230 with abnormal thyroid function tests from three hospital laboratories and 101 patients selected for normal thyroid function tests and normal glucose values. Participants were classified by TSH as euthyroid (n = 102), hyperthyroid pattern (n = 56) or hypothyroid pattern (n = 173). Spearman correlations, Kruskal–Wallis tests and robust linear regression were used, with multiple-imputation, threshold, restriction and sex-stratified sensitivity analyses. Results: In the whole cohort, TSH correlated with HbA1c (ρ = 0.59) and FPG (ρ = 0.63; both p < 0.001); median HbA1c was 5.1%, 5.8% and 6.6% in the euthyroid, hyperthyroid pattern and hypothyroid pattern groups. Within the hypothyroid pattern group, TSH was unrelated to HbA1c (ρ = 0.00) and FPG (ρ = 0.07), and overt and subclinical patterns had the same median HbA1c (6.6%). Thyroid function group alone explained 46% of HbA1c variance; continuous thyroid parameters, age, sex and body mass index explained 18%. Conclusions: The between-group differences and pooled correlations reflect a two-source design in which the comparison group was selected for normal glucose values. No graded relationship between thyroid function and glycemia was detectable within groups, and causal or directional inference is not supported.