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.

Background: The Duffy antigens Fy ^a and Fy ^b , encoded by ACKR1 (formerly DARC ), are absent from red cells in the Fy(a−b−) phenotype, which almost always arises from homozygosity for the FY *02N.01 GATA-box variant (rs2814778). It bears on two everyday problems in non-malignant hematology, red-cell alloimmunization and the interpretation of a low neutrophil count, and confers protection against Plasmodium vivax . Arabian data have been phenotypic and sparse. Objective: To assemble the Saudi and Gulf evidence on Duffy-null frequency and follow it into transfusion support, neutrophil reference intervals and vivax surveillance. Methods: PubMed and Web of Science were searched from July to September 2026, pairing Duffy, ACKR1 , DARC and rs2814778 with Arabian regional terms, neutropenia, reference intervals and alloimmunization. Confidence intervals are Wilson intervals recomputed from reported counts. Results: Provincial Fy(a−b−) frequency ranges from 26.7% in the north to 78.3% in Jazan, with Oman (68.5%) nearest and lower figures in the lower Gulf, consistent with enriched African ancestry at ACKR1 . In male Jazan donors the Duffy-null neutrophil interval was 1,140–5,290/µL and institutional limits classified 50.9% as neutropenic; isolated neutropenia reaches 21% locally. Duffy alloimmunization is documented at every Saudi center examined, exclusively as anti-Fy ^a , though the rates are not directly comparable. Conclusion: Jazan carries among the highest Duffy-null frequencies reported outside sub-Saharan Africa, with direct consequences for transfusion support and for neutrophil reference intervals. One western Saudi cohort has been genotyped at the FY promoter; the southwest, where frequencies are highest, has not, and closing that gap is the most tractable next step.

Background/Objectives: Thyroid hormone regulates erythropoiesis, but most population studies have used thyrotropin (TSH) alone and have not examined whether the erythroid association differs by red cell phenotype. We examined this in a population where inherited microcytosis and iron deficiency are both common. Methods: We analyzed 3871 adults of both sexes with paired free triiodothyronine (FT3), free thyroxine, TSH, and complete blood count from three hospitals in Jazan, Saudi Arabia (3673 with FT3 within the reference interval formed the primary analysis). All three analytes were entered simultaneously in models adjusted for age and sex; mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH) were pre-specified comparison (negative control) outcomes; red cell discriminant indices were used to assign a normocytic, acquired microcytic, or presumed inherited-trait pattern, which was compared against linked ferritin and transferrin saturation. Results: FT3 was associated with erythrocyte count (standardized β 0.097, 95% confidence interval (CI) 0.066–0.128, p < 0.001) and hemoglobin (+2.7 g/L per pmol/L); TSH was not (p = 0.547). The erythrocyte count association was present in normocytic (β 0.101) and acquired microcytic records (β 0.099) but absent in the presumed trait pattern (β −0.017; interaction p = 0.002) and remained absent under a stricter trait definition, whereas the hemoglobin association did not differ by phenotype (interaction p = 0.639). FT3 was unrelated to iron status, and the association survived adjustment for ferritin and restriction to same-episode iron measurements. In an exploratory comparison, both associations were strongest in iron-replete normocytic patients (hemoglobin +3.6 g/L per pmol/L, p < 0.001) and attenuated in measured iron deficiency. Conclusions: FT3, not TSH, was associated with erythrocyte count and hemoglobin. The count association was absent in the index-defined trait pattern, in which erythrocyte number is already high, and both associations were blunted where iron was limited. These observations are consistent with, but do not demonstrate, a limit on the marrow’s count response, since erythropoietic activity was not measured; they are hypothesis-generating and require replication with confirmed hemoglobin genotype, measured iron status, and reticulocyte or erythropoietin data.

Background/Objectives: Thyroid hormone regulates erythropoiesis, but most population studies have used thyrotropin (TSH) alone and could not ask whether the erythroid response depends on the marrow's capacity to respond. We examined this in a population where inherited microcytosis and iron deficiency are both common. Methods: We analyzed 3871 adults of both sexes with paired free triiodothyronine (FT3), free thyroxine, TSH, and complete blood count from three hospitals in Jazan, Saudi Arabia (3673 with FT3 within the reference interval formed the primary analysis). All three analytes were entered simultaneously in models adjusted for age and sex; mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH) were pre-specified negative controls; discriminant indices assigned red cell phenotypes, validated against linked ferritin and transferrin saturation. Results: FT3 was associated with erythrocyte count (standardized β 0.097, 95% confidence interval (CI) 0.066–0.128, p < 0.001) and hemoglobin (+2.7 g/L per pmol/L); TSH was not (p = 0.547). The erythrocyte count association was present in normocytic (β 0.101) and acquired microcytic records (β 0.099) but absent in the inherited-trait pattern (β −0.017; interaction p = 0.002) and remained absent under a stricter trait definition. FT3 was unrelated to iron status, and the association survived adjustment for ferritin. In an exploratory comparison, both the count and hemoglobin associations were strongest in iron-replete normocytic patients (hemoglobin +3.6 g/L per pmol/L, p < 0.001) and attenuated in measured iron deficiency. Conclusions: FT3, not TSH, was associated with the erythron, and the response was absent where erythrocyte number is constitutionally elevated and blunted where hemoglobinization is iron-limited. These hypothesis-generating findings require replication with confirmed hemoglobin genotype.