When Belding Scribner solved the long term dialysis access problem of chronic dialysis with the Scribner Teflon Shunt, the biggest hurdle was cleared. Unfortunately, “Scrib’s” very first chronic dialysis patient, Clyde Shields, suffered several severe and potentially life threatening complications shortly after beginning dialysis. Scribner had a dying patient in front of him even with his lifesaving vascular access allowing prolonged "chronic dialysis" and no prior case reports or studies on how to manage a chronic renal dialysis patient. Scribner, literally wrote the book on how to perform chronic dialysis well. Ironically, Scribner learned the most and was challenged the most with Clyde, his first patient. We have all benefited from what Clyde suffered and Scribner empirically got right.
Using reason, logic and empiric trials based on the evidence in the medical literature applied at the bedside, Scribner filled in the knowledge gaps immediately in a way that still applies to all dialysis patients that have followed even decades later. Here is short summary of some of the complications that Clyde Shields developed and Scribner and his team at Seattle found enduring solutions for that still apply today.
1) Clyde first developed Malignant Hypertension with very poor treatment options. (ganglion-blocking agents and reserpine)
Scribner instituted instead an empiric treatment of 400 mg/day sodium dietary restriction and aggressive ultrafiltration which quickly normalized Clyde’s BP and saved his life.
Scribner applied what he learned with Clyde to all of his patients, thus bringing forth the Drug Free Dry Weight method of BP control which is still the only successful treatment of ESRD patients on dialysis which is mainly a manifestation of the expanded Extracellular space due to excessive intake of sodium in the diet. Sadly, patients sometimes receive a sodium load even in dialysis with sodium levels often higher than the average patients plasma sodium levels. Thus, even at times in dialysis, they receive a net sodium gain and return home thirsty and unable to control their fluid intake. The average sodium level in the 1940’s with Kolff was 126.5 with 18 gm of Glucose to create a gradient to draw fluids. During the 1960’s and 1970's, it rose to 130-135 but now is as high as 149 in unusual circumstances with 140-141 very common.
Many studies show that a dialysate sodium levels of 140 often gives a sodium load leading to interdialytic weight gain (IDWG), increased thirst and the entire cycle of HTN followed by dramatic drops from excessive ultrafiltration during short treatments of 3-4 hours. Scribner’s dry weight method and matching the dialysis sodium to the serum sodium dramatically eliminates significant weight gain between sessions as my own case demonstrates. Sadly, the nephrology community at large has cast out all that Scribner learned, applied to his Drug Free Dry Weight method and that was replicated across the globe, most notably in Tassin France with Bernard Charra. Charra garnered over 95% Drug Free Dry Weight BP control within a few weeks of patients entering his clinic.
Weight in Kg (MAP)
Despite mountains of evidence accumulated by Scribner, Blagg and Kjellstrand and then replicated by Bernard Charra with over a combined 40 years of evidence of low sodium, probing dry weight with Ultrafiltration, the nephrology community struggles today to resolve the persistent hypertension plaguing patients and leads to high rates of cardiovascular events caused mainly by short, infrequent dialysis, poor adherence to low sodium diets and sodium loading during dialysis that is avoidable.
Blood pressure and volume management in dialysis: conclusions from a
Kidney Disease Improving Global Outcomes (KDIGO) Conference
Strategies aimed at improving vascular compensation and/or tolerance of UF may also lower the risk of UF-induced intradialytic hypotension and are listed in Tables 4and 5. Altering dialysate sodium concentration is the most debated approach (Table 5). Prospective studies suggest that use of lower dialysate sodium is associated with lower IDWG and BP90,91 but also show an association with intradialytic hypotension and symptoms, including cramps.92 Observational studies have yielded mixed results regarding the association of dialysate sodium and mortality.93, 94, 95 The Sodium Lowering in Dialysate (SoLID) RCT96,97 assesses the effects of low versus standard dialysate sodium concentration on regression of left ventricular mass, with results pending. Therefore, the ideal dialysate sodium concentration remains uncertain. A large multinational, pragmatic trial is ongoing (RESOLVE, NCT02823821). Moreover, the prescribed and delivered dialysate sodium concentrations can differ, rendering individualization of prescriptions challenging and potentially unsafe.98 In general, sodium balance should be negative during an HD treatment,1 given the tension between enhanced vascular space viability during a single treatment and lower IDWG across many treatments.
Clyde suffered several other acute conditions which had not been faced previously, for which Scribner treated as manifestations of uremia. He increased TIME and/or Frequency resolving all of these issues along with application of new meds for deficiencies and physiologic alterations not seen before.
2) Gout like arthritis: Scribner reasoned that Clyde needed further dialysis and went to thrice weekly 8-10 hours.
3) Metastatic calcification. Scribner spoke with a GI colleague in the hallway who noted Aluminum antacids lower phosphorus levels dramatically thus starting the use of phosphorus binders. The Aluminum toxicity was not recognized for many years after but it completely cured the metastatic calcification issues. Synthetic Vit D was not available until the early 1970’s.
4) Uremic Neuropathy. This was another serious and potentially life threatening condition when it involves autonomic peripheral nerves, that Clyde developed fairly early in his course. Scribner again, with little evidence in the medical literature to guide him, concluded he had inadequate dialysis and hypothesized that the neuropathy could be relieved by increasing the frequency and duration of dialysis. They also began supplementing the water soluble vitamins at this time. Scribner measured the response to a higher dose of dialysis with serial nerve conduction studies, correlating his response to the higher dose with the velocity of his nerve conduction. Scribner then applied this as his measure of adequate dialysis dosage all his patients:
"Eventually, motor nerve conduction velocity measurements became the guideline to ensure minimum adequate dialysis!"
This turns out to still be the most objective clinical measurement of “adequate” dialysis we have today in 2023. There are dozens of studies over the last two decades on uremic neuropathy corresponding to a measure of dialysis adequacy still in use today.
Effect of hemodiafiltration on the progression of neuropathy with kidney failure:
A randomized controlled trial
So, with Scribner’s first chronic hemodialysis patient, Clyde Shields, he devised an empiric treatment schedule of 8 hrs 3 times a week which matches kinetic modeling studies decades after he deduced this schedule at the patients bedside with clinical parameters alone. In addition, again at the patients bedside, using the powerful tools of logic and empiric trials, Scribner gave Clyde Shields 11 years of borrowed time, guiding him through several severe complications. This occurred without any RCT’s or prior case reports, but by his own clinical judgement and Clyde's response to empiric treatments. Scribner further defined one of the most sensitive objective measures of dialysis adequacy still in use today by monitoring effectiveness of the dosage of dialysis with nerve conduction studies and resolution or arrest of uremic neuropathy progression in 8/11 of his patients. He accomplished remarkable results still relevant today over 60 years later that are largely forgotten, or perhaps deliberately ignored. I am not sure which is operative. But the results are the same.
Patients suffer now while unending and often contradictory studies delay definitive treatment. Scribner stayed at the patients bedside with empiric trials until he discovered what worked in his very first patient. Otherwise Clyde would have been crippled and died many years before his eventual demise 11 years later. He did not abandon his patient to study an issue for 10 years as in the "failed" FHN Nocturnal study, and then debate the issue and validity of a failed study for another 10 years.
It is time to remember the tools of a bedside clinician walking through the sufferings of their patients with them, making decisions that in the case of Clyde Shields, were instructive to all ages.
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