Chronic kidney disease (CKD) is a serious public health problem in India,

affecting 13.4% to 15.4% of the population. In India, diabetes and hypertension account

for 40-60% of instances of Chronic Renal Failure. A steady decline in kidney function

causes end-stage renal disease (ESRD). Regardless of the underlying aetiology of

kidney illness, chronic renal failure is defined by a progressive loss of renal function.

Although proteinuria, poor control of hypertension, and diabetes are major risk

factors for chronic kidney disease progression to end stage renal disease, identifying

new risk variables could help in the goal of reducing end stage renal disease.

A main drop in serum bicarbonate concentration can occur when renal function

is compromised. Previously termed uremic acidosis, this disorder is more appropriately

called the metabolic acidosis of chronic kidney disease (CKD) because it is usually

unaccompanied by signs or symptoms of uremia.

The serum anion gap is defined as the sum of serum chloride and bicarbonate

concentrations minus serum sodium concentration, (Na+ + K+) - (Cl- + HCO3-) = 𝐀𝐧𝐢𝐨𝐧 𝐆𝐚𝐩;

as determined from electrolytes collected in a chemical laboratory. This entity

is employed in the detection and analysis of acid-base diseases, the evaluation of quality

control in chemical laboratories, and the detection of disorders such as multiple

myeloma, bromide intoxication, and lithium intoxication. The normal value can vary

significantly due to variances in the methods used to measure its elements as well as

significant interindividual variability. Low readings usually suggest a laboratory error

or hypoalbuminemia, but they can also indicate the existence of a paraproteinemia or

lithium, bromide, or iodide intoxication. Metabolic acidosis is the most prevalent cause

of elevated readings, but they can also be caused by laboratory mistake, metabolic

alkalosis, hyperphosphatemia, or paraproteinemia.

Although serum or plasma electrolytes can be used to compute the anion gap,

serum measurements are more commonly used. circulating cations (sodium, potassium,

calcium, magnesium, and cationic proteins) must equal circulating anions (chloride,

bicarbonate, anionic proteins, inorganic phosphate, sulphate, and organic anions). Only

the cations sodium and potassium, as well as the anions chloride and bicarbonate, are

commonly measured, hence the remaining cations and anions are referred to as

unmeasured cations (UC) and anions (UA), respectively. 

Although it is widely understood that uremia increases the serum anion gap

(AG), it was unknown whether alterations in the anion gap occur earlier in the course

of chronic renal disease. However, according to a study conducted by the International

Society of Nephrology, higher levels of anion gap are found in people with less

advanced kidney disease than previously thought, and are linked to an increased risk of

mortality.

From the electrolytes, the serum anion gap (SAG) can be simply computed. It

can be used to check laboratory quality control and diagnose intoxications and

paraproteinemias, in addition to differential diagnosis of acid-base diseases. Recent

research has revealed that serum anion gap could be used as a biomarker in a wider

range of situations. Even in the early stages of renal disease, serum anion gap levels are

higher and linked to mortality, and high serum anion gap levels are linked to chronic

kidney disease development. As a result, it’s thought that serum anion gap could predict

mortality in patients with severe chronic kidney disease.

In non-dialysis patients with end stage kidney disease, the traditional anion gap

equation commonly misdiagnoses a high anion gap state. Before the development of

Renin-angiotensin-aldosterone system (RAAS) inhibitors, the standard anion gap

equation was formulated more than half a century ago. Patients with end stage kidney

disease nowadays have a variety of comorbidities and have received a variety of

treatments, all of which may have an impact on the traditional anion gap value. If

clinicians calculate anion gap values for non-dialysis patients with end stage kidney

disease, they should be vigilant of any drugs, incidental inflammatory findings, and

estimated glomerular filtration rate (eGFR) that may have an impact on anion gap level.

If end stage kidney disease patients have non-high traditional anion gap values, we

advocate utilising a more accurate anion gap equation.

Chronic kidney disease (CKD), which causes progressive loss of kidney

function, is a serious public health issue in India that has yet to receive adequate

attention, as seen by the paucity of large-scale research in the country.(8)

Predicting who is at risk for chronic kidney disease is a crucial first step in

slowing down the disease’s progression. Early detection of chronic kidney disease

would allow for the most effective implementation of existing therapies for slowing the

loss of renal function.

According to The Multiple Risk Factor Intervention Trial (MRFIT) Research Group,

testing for an impaired GFR detects only 13% of patients who go on to develop end

stage renal disease, screening for proteinuria detects only 19%, and screening for both

detects only 27%. These findings, together with those from a recent study by Boulware

et al., show that screening for dipstick proteinuria by general practitioners is not costeffective

in terms of preventing end stage renal disease.

Beyond serum creatinine, nephrologists caring for severe chronic kidney

disease patients currently have no conveniently available indicators. Albumin adjusted

serum anion gap (A-SAG) can be a cost-effective and efficient guidance in this regard.

Clinicians can warn a patient with A-SAG > 9.48 mmol/L of a bad prognosis based on

prior study findings and advocate stricter adherence to medication and a healthy

lifestyle, as well as more frequent clinic visits for early interventions. Further research

into the most effective technique to lower albumin adjusted anion gap and the efficacy

of albumin adjusted anion gap lowering interventions is needed.

In Homoeopathy, a person is treated as a whole; in other words, the patient in

sickness is treated, not the disease in the patient. We analyse psychological, physical,

and pathological elements to find the most similar medicine that addresses all the

symptoms of the patient as a whole. As a result, the management of this disease state is

important, and Homoeopathy can play a vital role in reducing the morbidity and

slowing down the progression.

No relevant studies are conducted so far with regards to the effectiveness of

Homoeopathic treatment in bringing about favourable changes in the anion gap.

Therefore, in this study, I am intending to assess the anion gap in patients suffering

with/ at risk of chronic kidney disease and studying the effectiveness of Homoeopathic

Medicines in preventing its further progression.

Is Homoeopathic treatment effective in improving the anion gap in patients with

mild to moderate Chronic Kidney Disease and thereby preventing the disease

progression?

To study the role of Homoeopathic medicines in improving the anion gap in

patients with mild to moderate Chronic Kidney Disease and thereby preventing the

disease progression.

1. To see the effectiveness of Homoeopathic medicines in bringing the anion gap

to the normal range in patients with mild to moderate chronic kidney disease

thereby preventing/slowing its progression.

There will be no difference in the anion gap in patients with mild to moderate

chronic kidney disease after Homoeopathic treatment.

There will be a significant difference in the anion gap in patients with mild to

moderate chronic kidney disease.