Kidney disease is another reason to prevent metabolic syndrome

Summary: the insulin receptor resistance and higher insulin levels of metabolic syndrome are a significant risk factor for kidney disease.

We’ve long known that the kidneys are exquisitely sensitive to damage from higher levels of insulin. A study recently published in the Clinical Journal of the American Society of Nephrology further reveals the contribution metabolic syndrome to chronic kidney disease. Since MetS is on the rise, chronic kidney may too. The authors state:

“Observational studies have reported an association between metabolic syndrome (MetS) and microalbuminuria or proteinuria and chronic kidney disease (CKD) with varying risk estimates. We aimed to systematically review the association between MetS, its components, and development of microalbuminuria or proteinuria and CKD.”

The authors undertook an analysis of eleven studies encompassing 30,146 subjects that reported the development of microalbuminuria or proteinuria and/or CKD in subjects with MetS, with attention to eGFR (estimated glomerular filtration rate, a metric for kidney function). Their data present a clear picture:

MetS was significantly associated with the development of eGFR <60 ml/min per 1.73 m2 [impaired kidney function]. The strength of this association seemed to increase as the number of components of MetS increased. In patients with MetS, the odds ratios for development of eGFR <60 ml/min per 1.73 m2 for individual components of MetS were: elevated blood pressure 1.61, elevated triglycerides 1.27, low HDL cholesterol 1.23, abdominal obesity 1.19, and impaired fasting glucose 1.14. Three studies reported an increased risk for development of microalbuminuria or overt proteinuria with MetS.”

The ‘take home’ message for clinicians and patients is don’t wait until the onset of type 2 diabetes; bear in mind the authors’ conclusion and take decisive action before delicate kidney tissue is irrevocably lost:

MetS and its components are associated with the development of eGFR <60 ml/min per 1.73 m2 and microalbuminuria or overt proteinuria.”

Microscopic blood in the urine can be a risk for severe kidney disease

Trace amounts of blood cells in the urine without symptoms is often dismissed, but a study just published in JAMA (The Journal of the American Medical Association) offers evidence that asymptomatic microscopic hematuria can be a risk factor for serious kidney disease requiring dialysis and/or transplant. The authors set out to…

“…evaluate the risk of end-stage renal disease (ESRD) in adolescents and young adults with persistent asymptomatic isolated microscopic hematuria.”

They conducted a cohort study using medical data from 1,203,626 subjects, male and female, who were examined for for the Israeli military services, with reference to the Israeli treated ESRD registry. They were then able to estimate the hazard ratio (HR) of treated ESRD among those diagnosed as having persistent asymptomatic isolated microscopic hematuria. The outcome measure for ESRD was initiation of dialysis or kidney transplantation. What did the data show?

“A substantially increased risk for treated ESRD attributed to primary glomerular disease was found for individuals with persistent asymptomatic isolated microscopic hematuria compared with those without the condition (incidence rates, 19.6 vs 0.55 per 100 000 person-years, respectively; HR, 32.4).”

Although the overall incidence of ESRD among young adults is very low, when asymptomatic microscopic hematuria is detected by positive dipstick and confirmed by microscopic analysis, clinicians should be alert to the possibility of an underlying (likely autoimmune) process that could evolve into ESRD by bearing in mind the authors’ conclusion:

Presence of persistent asymptomatic isolated microscopic hematuria in persons aged 16 through 25 years was associated with significantly increased risk of treated ESRD for a period of 22 years, although the incidence and absolute risk remain quite low.”

 

 

Risk for high blood pressure, kidney and cardiovascular disease can persist long after E. coli gastroenteritis

Research just published in the British Medical Journal presents another example of acute gastrointestinal infection triggering chronic inflammation that persists long after the infection has subsided. The authors set out to…

“…evaluate the risk for hypertension, renal impairment, and cardiovascular disease within eight years of gastroenteritis from drinking water contaminated with Escherichia coli O157:H7 and Campylobacter.”

They followed 1977 adult participants, 1067 of whom came down with acute gastroenteritis when a municipal water system was contaminated. None of them had a history of the subsequent diseases they were looking for which included hypertension (blood pressure ≥140/90 mm Hg), kidney impairment (microalbuminuria or estimated glomerular filtration rate <60 ml/min/1.73 m2), and cardiovascular disease (heart attack, stroke, or congestive heart failure). What did the data show?

“The adjusted hazard ratios for hypertension and cardiovascular disease after acute gastroenteritis were 1.33 and 2.13 respectively. The adjusted hazard ratio for the presence of either indicator of renal impairment was 1.15 and was 3.41 for the presence of both.”

In other words, having a case of acute gastroenteritis resulted in a later increase of 33% in the risk for high blood pressure, 213% for cardiovascular disease, and a whopping 341% for a combination of the two indicators of kidney impairment (microalbuminuria and lower glomerular filtration rate). Thus the authors conclude:

Acute gastroenteritis from drinking water contaminated with E coli O157:H7 and Campylobacter was associated with an increased risk for hypertension, renal impairment, and self reported cardiovascular disease…Our findings underline the need for following up individual cases of food or water poisoning by E coli O157:H7 to prevent or reduce silent progressive vascular injury…annual blood pressure monitoring and periodic monitoring of renal function may be warranted for individuals who experience acute gastroenteritis after exposure to food or water contaminated with E coli O157:H7.”

This is another example of how GI infections can trigger the long-term immune system dysregulation that promotes chronic inflammation, the biological basis of cardiovascular disease and renal impairment. Clinicians should be diligent in diagnosing GI infection and astute in examining for immune dysfunction and occult autoimmune disorders.

Heart rate variability analysis predicts kidney disease

Journal of the American Society of NephrologyHere’s more evidence for the profound value of heart rate variability analysis and the fundamental importance of the regulation of functions throughout the body by the autonomic nervous system. In a study just published in the Journal of the American Society of Nephrology the authors investigated the correlation between HRV and chronic kidney disease (CKD):

Autonomic imbalance, a feature of both diabetes and hypertension, may contribute to adverse cardiovascular outcomes. In animal models, sympathetic nerve activity contributes to renal damage but the extent to which autonomic dysfunction precedes the development of CKD and ESRD [end-stage renal disease] in humans is unknown.”

They measured a number of parameters of HRV analysis in a population of 13,241 adults for 16 years: and found 199 cases of ESRD and 541 patients of CKD; higher resting heart rate and lower heart rate variability was associated with both.

“Other time and frequency domain measures [of HRV] were similarly and significantly associated with ESRD and CKD-related hospitalizations. These results suggest that autonomic dysfunction may be an important risk factor for ESRD and CKD-related hospitalizations…”

It’s hard to think of a clinical test that is easier to perform yet yields more valuable information on the arousal state and capacity of the body to regulate its functions than the heart rate variability analysis.