Reversing Chronic Kidney Disease with Niacin and Sodium Bicarbonate

25 individuals with CKD (chronic kidney disease) stages 2-4 treated with a combination of supplements, including 500mg niacin 3x/day for three months, improved the disease by at least one stage.

Overview

This case series, published in the Orthomolecular Medicine News Service, reports on 25 patients with chronic kidney disease (CKD) at stages 2 through 4 who were treated with a combination protocol including 500 mg nicotinic acid (niacin) three times per day — 1,500 mg/day total — along with sodium bicarbonate and other supportive supplements. After three months, all 25 individuals improved by at least one CKD stage, and some improved by two stages.

Important: The study specifies nicotinic acid — the form of vitamin B3 that activates the GPR109A receptor and produces the characteristic niacin flush. Niacinamide (nicotinamide), the more common supplement sold as “niacin,” does not produce these effects and was not the compound studied.

What Is CKD?

Chronic kidney disease is defined by progressive loss of kidney function measured by estimated glomerular filtration rate (eGFR). The staging system:

• Stage 1: eGFR ≥ 90 (normal or high, with kidney damage markers)
• Stage 2: eGFR 60–89 (mildly reduced)
• Stage 3: eGFR 30–59 (moderately reduced)
• Stage 4: eGFR 15–29 (severely reduced)
• Stage 5: eGFR < 15 (kidney failure)

CKD is typically considered irreversible and progressive. Conventional treatment focuses on slowing the decline, not reversing it.

The Protocol

The combination treatment used in this case series:

• Nicotinic acid: 500 mg, three times daily (1,500 mg/day total)
• Sodium bicarbonate: to address metabolic acidosis, a common CKD complication
• Additional supportive supplements (detailed in the source publication)

Results

All 25 participants improved by at least one CKD stage over three months — a finding that stands out because conventional medicine treats CKD progression as a one-way decline.

Why Niacin May Help Kidneys

Several mechanisms may explain the benefit:

Phosphate reduction. Niacin reduces phosphate absorption in the gut. Elevated phosphate is a known driver of CKD progression and cardiovascular complications. Niacin functions similarly to pharmaceutical phosphate binders — standard CKD therapy — via a different pathway.

GPR109A activation. Nicotinic acid activates the GPR109A receptor, which has anti-inflammatory effects in multiple tissues. Chronic inflammation drives CKD progression, and GPR109A agonism may reduce some of this inflammatory burden. The same receptor activated by niacin in fat cells (causing the flush) is also expressed in kidney tissue and immune cells.

NAD+ precursor. Niacin is a precursor to NAD+, essential for cellular energy. NAD+ depletion is associated with acute kidney injury and chronic disease progression. Restoring NAD+ levels through nicotinic acid supplementation may support renal cell repair.

Limitations

This is a case series — observational, not a randomized controlled trial. With 25 patients and no control group, confounding factors cannot be excluded. Sodium bicarbonate alone can improve eGFR in acidotic patients, making it difficult to attribute improvement specifically to niacin. Larger controlled trials are needed.

Context in GPR109A Research

This case series fits within a broader literature on niacin’s systemic effects mediated through GPR109A. The same receptor that mediates the niacin flush is expressed in kidney tissue, intestinal epithelium, and immune cells — and its activation appears to have anti-inflammatory and cytoprotective effects across organ systems.