February 17, 2026
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Modern kidney medicine carries an aura of precision. Dialysis targets are calculated to the decimal. Lab reports arrive with staged classifications. Protocols are presented as if debate ended long ago. Yet beginning around 2000, nephrology became dominated by the guideline movement—much of it shaped by pharmaceutical-funded groups. Once incorporated into treatment protocols and performance measures, these guidelines began to influence practice in ways that discouraged clinical reasoning, creative thinking, and even research itself. The presence of a guideline began to signal that the science was settled.
Nephrology was once considered the “thinking” subspecialty—rooted in chemistry, acid–base balance, and fluid physiology. Managing dialysis and transplant patients requires expertise across cardiology, hematology, bone metabolism, and endocrinology. These patients are fragile. Hospitalizations are frequent. Mortality remains high. The stakes are not theoretical.
In the 1980s, the theory that restricting dietary protein would slow chronic kidney disease gained traction, largely extrapolated from rat models. The concept was appealing enough to trigger the large NIH-funded MDRD trial. Over 800 patients were enrolled. Kidney function was measured rigorously. The results were clear: protein restriction did not significantly slow disease progression. In the very low protein group, signs of malnutrition appeared.
The hypothesis had failed.
Yet the mythology persisted. Re-analyses attempted to reinterpret the data after the fact. Conferences continued promoting highly restricted diets. Meanwhile, attention drifted away from a more powerful intervention: addressing type 2 diabetes, the leading cause of chronic kidney disease. In clinical practice, reversing diabetes often stabilizes or improves diabetic kidney disease. That reality received far less institutional enthusiasm.
The MDRD study also produced something else: an equation to estimate kidney function from serum creatinine. The estimated GFR became automated, attached to every lab result. Soon after, the National Kidney Foundation built a staging system around it.
This classification labeled millions of otherwise healthy individuals—especially older adults—with chronic kidney disease based largely on mathematical adjustment. Kidney function declines with age. The formula guaranteed that many elderly patients would be staged as diseased. That label often triggered early dialysis preparation and early placement of vascular access, even when conservative management might have safely delayed intervention for years.
Race adjustments once attempted to account for muscle mass differences in African American patients. Those adjustments were later removed, instantly altering transplant eligibility patterns. A mathematical modification carried real-world consequences.
The arteriovenous fistula revolutionized hemodialysis by enabling adequate blood flow for treatment. But as surgical techniques shifted toward larger, higher-flow fistulas in the upper arm, a new problem emerged.
Oversized fistulas create large left-to-right shunts, sometimes exceeding two liters per minute. The heart must continuously pump that extra volume. Over time, this leads to chamber enlargement, pulmonary hypertension, high-output heart failure, and ultimately cardiomyopathy. Peripheral circulation suffers. Malnutrition and systemic decline follow.
The fistula became beloved within dialysis culture. “Fistula first” became a movement. Yet a fistula is a non-physiologic anomaly. Small, carefully constructed wrist fistulas—like those commonly created by Japanese surgeons—achieve sufficient blood flow with far less cardiac burden. Not coincidentally, Japanese dialysis patients demonstrate superior longevity.
A lifeline, if oversized, can become lethal.
Bone complications are nearly universal in advanced kidney disease because the kidneys regulate calcium, phosphorus, and vitamin D. During the 1990s, aluminum-related bone disease was eliminated by stopping aluminum-based phosphate binders. But new problems emerged.
Calcimimetic drugs such as cinacalcet were promoted aggressively through guideline panels funded by industry. The drug suppresses parathyroid hormone (PTH), but its complex effects on different PTH fragments raised concerns about over-suppression and reduced bone turnover. Independent analyses suggested that bone metabolism was being altered in ways not fully disclosed in industry-sponsored publications.
Meanwhile, bisphosphonates—drugs commonly used for osteoporosis—were recommended for dialysis patients based on bone density scores. Yet bone density testing does not reflect the complex bone disorders of kidney failure. In biopsy studies, 100% of dialysis patients treated with bisphosphonates developed adynamic bone disease. These drugs accumulate indefinitely in kidney failure and can weaken bone further.
The guidelines advanced. The science behind them remained fragile.
The introduction of recombinant erythropoietin (EPO) transformed nephrology. Hemoglobin levels rose. Fatigue improved. Enthusiasm surged. Guidelines—funded entirely by the drug’s manufacturer—recommended increasingly aggressive targets.
But hemoglobin is a concentration, not a total red blood cell mass. Dialysis patients are often volume overloaded before treatment. Excess fluid dilutes hemoglobin and albumin levels, creating the illusion of anemia and malnutrition. Dosing EPO based on these diluted values led to escalating drug use.
Large trials eventually revealed the cost. Targeting near-normal hemoglobin levels increased cardiovascular events, stroke, access thrombosis, and mortality. The “normal hematocrit trial,” CHOIR, CREATE, and TREAT studies all demonstrated harm at higher targets.
The alternative explanation is simpler: volume overload, not true anemia, drives poor outcomes. Sodium and fluid excess strain the heart. Controlling volume improves survival. Chasing hemoglobin numbers may worsen it.
For years, EPO was reimbursed separately, creating financial incentives tied directly to higher dosing. The economic structure reinforced the medical momentum.
Dialysis can sustain life for years. Without it, patients with end-stage kidney failure die. Yet within dialysis practice, certain traditions—oversized fistulas, aggressive anemia targets, bone drug overuse—have introduced avoidable harm.
The common thread is not technology itself, but uncritical acceptance of guideline-driven practice, especially when shaped by industry influence. In a discipline once defined by careful bedside reasoning, reclaiming that mindset may be the most important intervention of all.
