I’m reading the January NephSAP on primary care for the working nephrologist

There is some great stuff in there. This line on the futility of cancer screening among dializers struck me as particularly interesting:

[Kajbaf et al.] calculated the maximum increase in life expectancy (for a 60-yr-old woman) from routine Papanicolaou (Pap) testing and mammography to be 3 and 2 days, respectively.

Wow. (Ref PDF)

I feel like dialysis is always geting beat up over the high yearly mortality rate, and admittedly it is high. So it was interesting to see this table of some other conditions and there associated mortality. I didn’t realize dialysis had such familiar company.

The highest aldosterone I have ever seen

Patient came to me with hypokalemia and hypomagnesemia. She had been asymptomatic when she underwent routine pre-op labs for an elective procedure. Her potassium was 2.0 and the magnesium was later discovered to be 0.9 mmol/L.

She had been treated for 5 months with supplemental potassium and magnesium before she found her way into my office.

During her initial work-up we found:

  • Aldosterone: 61.2
  • Renin: 12.4
  • Trans-tubular potassium gradient: 15.98
  • Diuretic screen: negative
  • 24-hour urine calcium: 57 mmol

Her blood pressure was 120s over 80s on 5 mg of amiloride daily. Her volume status appeared essentially normal.

No renal vascualr disease by MRA, normal CT scan of the abdomen (no renin producing tumor). She was not on aldactone.

Diagnosis: Gitelman’s syndrome.

The principle characteristics of Gitelman’s are: low potassium, low magnesium, initially presenting in adolescence or adulthood. Patients have normal growth. Blood pressure is low. When I first learned about Bartter’s and Gitelman’s I imagined them as congentital diuretics:

  • Bartter’s is congenital Lasix
  • Gitelman’s is congenital HCTZ
The conditions can be understood nearly completely with this crude model. They both have low blood pressure as can be expected from a diuretic-like action. The low blood pressure triggers the renin-angiotensin-aldosterone system resulting in high plasma levels of renin and aldosteronism. In primary hyperaldosteronism, renin is suppressed.
Increased distal delivery of sodium along with increased aldosterone levels leads to increased potassium and hydrogen wasting leading to metabolic alkalosis and hypokalemia.

The two diseases differ in a few areas. Bartter’s results in decreased concentrating ability while concentrating ability is generally intact in Gitelman’s. This is predictable as the Loop of Henle is the engine which drives urinary concentrating and diluting ability. Gitelman’s has a low urinary calcium just as found with thiazides.

What was remarkable to me, was how high the aldosterone level was. This is in a patient without adrenal disease, the aldosterone is released in response to normal stimuli, volume depletion in this case. In primary aldosteronism, where there is autonomous secretion of aldosterone by a tumor, the aldosterone level typically rises to 20-30. But in this patient, where the adrenal gland is intact, the aldo level goes bonkers to almost 70.


My Grand Rounds

For the last 6 weeks I have been pounding the computer finishing and perfecting my lecture which I gave at Grand Rounds at both Providence Hospital and St John’s Hospital.

I delivered the second one yesterday.

Here is the lecture with an audio track. My presentations are not self-contained most of the important data comes from me presenting. I hope you like it. (.zip file of native Keynote file)

Reading Atul Gawande’s Checklist Manifesto

Reading The Checklist Manifesto is a mind expanding experience. I can’t stop thinking about its implications and how I can help my patients by eliminating “errors of ineptitiude.” (Which I learned as the difference between errors of omission as opposed to errors of cognition, where the latter is an error because the condition requires care beyond the skill level of the individual and the former is when the patient is harmed because of a lapse in applying standard care.)

Good blog post on the Gawande. A negative review of the book in the Wall Street Journal. A positive review on Amazon by Malcolm Gladwell.

My emphasis on teaching as my personal niche in medicine is from the idea that more important than pushing boundries of science is to learn the lessons of what has already been discovered.

After reading a couple of chapters I searched for Gawande in the NEJM and was delighted to see the breadth of contributions he has made as either scientist, editorialist or subject.

Right now I am busy crafting checklists for nephrology. I am focusing on the outpatient CKD care and routine admissions for hemodialysis patients.
Is anyone aware of checklist implementation in nephrology?

Monitoring therapeutic Dilantin in renal failure requires looking at the free not total Dilantin.

My fellowship director was the Great Brain, Dr Patrick Murray. Pat is quadruple boarded:

  1. internal medicine
  2. critical care
  3. nephrology 
  4. clinical pharmacology

Pretty intimidating. (If you have the time, check out his 179-slide presentation. Wow!)

One of the side effects of doing my fellowship under a professor in clinical pharmacology is that I learned more about drug monitoring in renal failure than any innocent nephrology fellow should.

One of the pearls he taught regarded the monitoring of therapeutic Dilatin (phenytoin) levels. the Renal Fellow Network discussed Dilantin pharmacokinetics twice but neither of the posts noted the change in protein binding that occurs with renal failure.

Dilantin is highly protein bound (90%) and only the free dilantin is therapeutically active. Uremia is associated with plasma molecules which displace Dilantin from albumin. This increases the active fraction of Dilantin, so sub-therapeutic total levels of Dilantin may represent appropriate free levels in the presence of renal failure.

I currently have a dialysis patient in the ICU who was seizing following a cardiac arrest. He was loaded with Dilantin and a few days later his labs showed:

Total phenytoin level of 5 mcg/mL, below the therapeutic target of 10-20. Simultaneously his free level was 1.14 mg/L. (Rant: How can the EMR express the total level as mcg/ml and the free level as mg/L. THEY ARE EQUIVALENT. Don’t hide it.)

So in this case the free dilantin is 23% of the total, rather than the normal 10%. Note that the total level appears sub-therapeutic but this patient would be poorly served by a re-loading of Dilantin as his free level is therapeutic.

Summary: in uremia always use the free dilantin level and don’t trust the total Dilantin level.

Funniest thing a patient sent me

I just got this e-mail from a patient and felt compelled to share one short bit:

…i consider you a good friend and the
greatest doctor of all time (well, maybe
Dr. Frankenstein was a little better.  he
did after all assemble from corpse parts
a human entity and brought it to life.
trying topping that one Dr.Topf).