Bilirubin Impact on Diabetic Kidney Disease

Shiva Mani^*
*Correspondence: Shiva Mani, Department of Medicine & Advanced Technology, Seoul National University Hospital, Seoul, Korea, Email:

Introduction

In the past, it was thought that bilirubin was either a non-functional by product of heme catabolism, a sign of liver disease, or, worst of all, molecules that could be harmful to the brain. It is reasonable to assume that bilirubin is more than just a byproduct of heme catabolism because mammals expend energy and resources converting biliverdin, a non-toxic compound that is relatively simple to secrete, into bilirubin, which must be further metabolized for excretion or a biliary system. Numerous DKD-related biomarkers have been identified. However, their use in clinical settings is limited because most of them have not been clinically tested. The connection between IgG and kidney disease has recently received a lot of attention. An increase in IgG excretion rate in nephropathy has been shown to indicate a decrease in the estimated glomerular filtration rate (eGFR) and an increase in segmental glomerulosclerosis, which may indicate the progression of the disease. IgG levels in the urine are a sign of severe glomerular damage and proteinuria. IgG levels in the urine can rise before micro albuminuria develops, according to studies. We excluded patients with a history of primary nephrotic syndromes, chronic glomerulonephritis, lupus nephritis, urinary tract infection, acute kidney injury, urinary calculi, polycystic kidney disease, renal tubular injury, gout-associated nephropathy, hypertensive nephropathy, pyelonephritis and interstitial nephropathy, such as gout.

CKD itself is a significant independent risk factor for cardiovascular disease (CVD), an additional diabetic co-morbidity. Diabetes and CKD have been linked to higher rates of hospitalization and mortality. Age, retinopathy, albuminuria, serum haemoglobin A1c levels, serum uric acid levels and anemia have been identified as independent risk factors for the development of CKD in diabetes. These risk factors make it easier to identify patients who are most vulnerable to disease progression, which in turn makes it easier to optimize care and improve patient outcomes. DKD is a multifactorial, complicated condition with environmental risk factors and genetic predisposition. As a result, more tools are needed to help identify this condition earlier and lessen its impact on patients and healthcare systems [1].

Description

Gilbert Subjects' mild hyper bilirubinemia, as well as levels in the upper quartiles of the currently accepted physiological serum bilirubin range, began to protect them from the rise in civilization diseases like cardiovascular disease, diabetes, obesity and metabolic syndrome, which are primarily caused by oxidative stress. In the meantime, basic scientists started looking into the mechanisms by which this molecule protects the body. They found that bilirubin is an important regulator of many biological processes in the human body and can act like a hormone by directly affecting its receptor. Scientists are thinking about increasing serum bilirubin levels as a way to prevent civilization diseases because it appears that a small increase in bilirubin levels significantly reduces the impact of oxidative stress-related diseases. About 20% to 40% of diabetics with type 1 or type 2 diabetes suffer from kidney disease (DKD). To stop DKD from progressing to end-stage renal failure, early detection is essential. The improvement of treatment and the development of methods to predict the progression of DKD are the current areas of study.

As a potential marker for progression and a therapeutic target for DKD prevention, endogenous bilirubin appeared to be significant. The total serum bilirubin level may be regarded as a marker of DKD progression based on a number of recent studies, which are well explained in this review, making it useful for identifying low-risk and high-risk patient groups. In order to avert kidney failure, patients with low–normal total bilirubin concentrations may be aggressively managed. As a marker, bilirubin can be easily, cheaply and frequently measured in most medical facilities. To determine whether total bilirubin concentration is a potential therapeutic target for CKD prevention, additional research is required. Changes in lifestyle, the use of natural compounds as nutraceuticals or chemical drugs and the inclusion of bilirubin in nanoparticles are some of the measures that can mildly raise serum bilirubin levels [2-5].

Conclusion

Its effects on the onset and progression of renal diseases have been demonstrated in recent basic and clinical studies, demonstrating that only slight or very slight increases in serum bilirubin concentrations provide real clinical benefits. As a potential marker for progression and a therapeutic target for DKD prevention, endogenous bilirubin appeared to be significant. To delay the onset of kidney failure, patients with low–normal total bilirubin levels may require more aggressive treatment. To determine whether total bilirubin concentration is a potential therapeutic target for CKD prevention, additional research is required. Several diseases caused by oxidative stress and inflammation, including DKD, are being considered for prevention by scientists by adjusting plasma bilirubin concentrations.

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