Association Between Plasma Homocysteine and Microalbuminuria in Untreated Patients with Essential Hypertension: a Case-Control Study

Abstract

Background/Aims: Kidney function is critical for homocysteine (Hcy) clearance, and plasma Hcy levels are frequently increased in patients with renal failure. Microalbuminuria (MAU) is an important marker of early renal damage caused by hypertension. At present, there is insufficient evidence on the relationship between Hcy and microalbuminuria. Methods: This is a 1: 2 matched, hospital-based case-control study. At initial visit, out of 1535 outpatients with no prior history of medication, 450 qualified subjects were selected based on inclusion and exclusion criteria. The concentration of Hcy in the serum was evaluated using a cyclic enzyme method. MAU was defined by a urine albumin/creatinine ratio (UACR) between 30 μg/mg and 300 μg/mg. Results: A total of 450 patients were included in this study (150 in the MAU group and 300 in the non-MAU group). The MAU group had higher mean systolic blood pressure (SBP), mean diastolic blood pressure (DBP), heart rate (HR) and plasma Hcy levels than did the non-MAU group. The area under the receiver operating characteristics (ROC) curves was 0.772 (95% CI: 0.724–0.819, P < 0.001) with a cut-off value of 15.0, and the sensitivity and specificity of Hcy in predicting the MAU status in hypertensive patients were 49.3% and 92.3%, respectively. Multiple logistic regression modelling suggested that patients with a higher Hcy level (> 15 µmol/L) were more likely to have MAU (95% CI: 5.650–16.543, P < 0.001). The other predictive factor for MAU was 24-h mean SBP (95% CI: 0.941–0.993, P = 0.015). Conclusion: This matched case-control study indicates that Hcy may increase the susceptibility of essential hypertensive subjects to MAU.

Genetically elevated circulating homocysteine concentrations increase the risk of diabetic kidney disease in Chinese diabetic patients

“…Homocysteine is a sulphur-containing non-proteinogenic amino acid biosynthesized from methionine and abnormal elevation of circulating homocysteine concentrations has been implicated in the development of many clinical end-points or pathological conditions, such as cardiovascular disease, 15 stroke 16 and microalbuminuria. 17 Hyperhomocysteinaemia is an independent risk factor for glomeruloslerosis and renal insufficiency and the association of circulating homocysteine with DKD was widely evaluated in the medical literature, yet the results are not often reproducible. [7][8][9][18][19][20][21][22] Actually, current evidence linking homocysteine to DKD is mainly based on observational data, in which the degree of possible confounding and reverse causation may cloud the true relationship.…”

Serum homocysteine is associated with tubular interstitial lesions at the early stage of IgA nephropathy

“…An animal study implicated elevated Hcy related to glomerular injury [ 26 ]. In both essential hypertension and general adult populations, high Hcy was associated with albuminuria independent of renal function [ 27 , 28 ]. A prospective study showed that Hcy was an independent determinant of the development of albuminuria even after adjustment for eGFR [ 29 ].…”

B cell-derived anti-beta 2 glycoprotein I antibody mediates hyperhomocysteinemia-aggravated hypertensive glomerular lesions by triggering ferroptosis

“…[3][4][5] HHcy has been identified as a risk factor of CKD and contributes to cardiovascular complications. [6][7][8][9] A cross-sectional survey reveals that hypertension is a major cause of CKD, 10 but the molecular mechanisms by which HHcy mediates hypertensionassociated kidney damage remains poorly understood.…”