As we come to the end of the naughts, we naturally reflect back and think about how far we have come from in the last ten years. Here is my quick list:
MYH9 gene for ESRD
The failure of the normalization of hemoglobin and the wholesale reevaluation of ESAs
The rise of aldosterone and its importance in hypertension and renal disease
the failure of dialysis dose to improve out come in both chronic (HEMO) and acute dialysis (ATN).
FGF-23, hey a whole new hormone and a major advancement in renal physiology
Re-emergence of home dialysis
Problems with the definition of CKD and the problems with eGFR
discovering the antigen in idiopathic membranous nephropathy
I want to do a longer article about this but I’m sure I’m missing some stuff. I don’t have a transplant subject, seems like vitamin D belongs up there, what about the phos binder wars? Bundling? What about MMF in lupus nephritis and every other GN?
I saw the highest glucose I can remember in a patient without ESRD. I have seen the glucose go over 2,700 in a patient with the misfurtune to have both DKA and anuric ESRD. Without the osmotic diuresis to lower the glucose the glucose can shoot the moon. This patient had HyperOsmolar Non-Ketotic Coma (or HONK as my fellow calls it, love that) and baseline Cr of 0.83 and a peak glucose of 1,600 mg/dL.
I love the twin graphs showing the falling glucose and the simultaneous resolution of the pseudohyponatremia. The patient had enough pre-existing osmotic diuresis to cause hypernatremia which was masked by the hyperglycemia. As the glucose comes down the sodium goes up from 136 to 162.
Calcium The other crazy number was the most severe hypercalcemia I have ever seen. The calcium was 18 mg/dL with an albumin of 3.7 g/dL. The patient is a kidney transplant recipient who was recently seen in the outpatient clinic with hypocalcemia. His calcium was 6.5 and his calcitriol was increased from 0.5 mcg to 1 mcg twice daily. He was also continued on his calcium carbonate.
Admission labs:
The other pertinent calcium labs:
PTH: 3.2 pg/mL
Vit D 1,25 dihydroxy: 36 pg/mL
SPEP/UPEP: unremarkable
PTHrp: pending
I think this is milk-alkali syndrome from the calcium carbonate exacerbated by the calcitriol. One supporting string of evidence supporting this is the fact that his calcium came down and has not reoccurred. If it was hypercalcemia of malignancy I would have expected his calcium to be resistant to conservative therapy.
Does removal of the light chains with plasmapharesis reduce the severity of cast nephropathy? We know that renal failure is a terrible prognostic factor in multiple myeloma so fixing acute renal failure is important.
Though not randomized this recent article from KI should be of interest (Thanks Kyste):
Leung et al. Improvement of cast nephropathy with plasma exchange depends on the diagnosis and on reduction of serum free light chains. Kidney Int (2008) vol. 73 (11) pp. 1282-8.
I was scheduled to give a talk on disorders of sodium and water to the fellows yesterday. We have a particularly clever cohort of fellows this year and I really couldn’t give them a warmed over version of my resident and student sodium lecture so I put together this talk which looks five different issues with hyponatremia and some data regarding them:
mannitol induced pseudohyponatremia
TURP syndrome
uremia and propensity for myelinolysis
exercise induced hyponatemia
differentiation of salt delpetion from SIADH with FENa, FEUrea and FE Uric acid with a couple of slides on treating SIADH with saline
Remember, downloading the native Keynote file will give you animations and a better looking experience.
Last Thanksgiving weekend, many bloggers participated in the first documented “blog rally” to promote Engage With Grace – a movement aimed at having all of us understand and communicate our end-of-life wishes.
It was a great success, with over 100 bloggers in the healthcare space and beyond participating and spreading the word. Plus, it was timed to coincide with a weekend when most of us are with the very people with whom we should be having these tough conversations – our closest friends and family.
The original mission – to get more and more people talking about their end of life wishes – hasn’t changed. But it’s been quite a year – so we thought this holiday, we’d try something different.
A bit of levity.
At the heart of Engage With Grace are five questions designed to get the conversation started. We’ve included them at the end of this post. They’re not easy questions, but they are important.
To help ease us into these tough questions, and in the spirit of the season, we thought we’d start with five parallel questions that ARE pretty easy to answer:
Silly? Maybe. But it underscores how having a template like this – just five questions in plain, simple language – can deflate some of the complexity, formality and even misnomers that have sometimes surrounded the end-of-life discussion.
So with that, we’ve included the five questions from Engage With Grace below. Think about them, document them, share them.
Over the past year there’s been a lot of discussion around end of life. And we’ve been fortunate to hear a lot of the more uplifting stories, as folks have used these five questions to initiate the conversation.
One man shared how surprised he was to learn that his wife’s preferences were not what he expected. Befitting this holiday, The One Slide now stands sentry on their fridge.
Wishing you and yours a holiday that’s fulfilling in all the right ways.
Turns out that seemingly sound advice will kill’ya.
Headlines from this week:
Any drinking lowered the risk of heart disease but the more patients drank the greater the protection. And the amount they drank was pretty staggering:
light drinking, about a glass of wine or 1.5-beers per day,reduced risk by 35%
moderate drinking, 2 glasses of wine or 2-3 beers reduced the risk 51%
Moderate and heavy drinking, 5+ glasses of wine or 7+ beers, resulted in 54 and 50% risk reduction.
The health benefits of alcohol were touched upon in ths prior post.
Not only did the patients randomized to folic acid + B12 have a higher rate of developing cancer, they had a higher cancer mortality. Most of the cancer mortality came from excess lung cancer in the folic acid + B12 group. This was despite the fact that there were more smokers in the placebo group (38% vs 40% p=0.01). (JAMA)
The fall of folic acid was touched on in this prior post.
So parents, remind your kids to drink their beer and forget their vitamins.
I have a patient with nephrotic syndrome, renal vein thrombosis and two pulmonary embolisms in the last year. I told him that the nephrotic syndrome was likely due to membranous nephropathy and that all of his various blood clots are due to the kidney disease. The biopsy came back today and it is indeed membranous nephropathy.
Membranous nephropathy is a common finding when patients are biopsied for nephrotic syndrome. Fortunately, it is a relatively benign disease with a significant number of spontaneous remissions. (Schieppati, NEJM 1993)
Adequate renal function was defined as “no ESRD”
Since there are so many spontaneous remissions and the therapy has significant side-effects we risk stratify patients in order to spare low-risk patients from treatment.
greater than 8-10 g/day for more than 6 months (PDF)
increased serum creatinine (Cr over 1.5) (Medline)
Though the instinct after getting a kidney biopsy is to start therapy immediately, in patients with a normal creatinine, waiting for 6 months and monitoring the creatinine and proteinuria does not alter the patients response to treatment. (Medline)
The biopsy findings have long been held of major importance on predicting prognosis but an analysis of 389 biopsies questioned whether histology provided information that independently predicted prognosis. (Medline)
Two urinary findings are gaining acceptance at being able to better predict the clinical course of disease. Beta-2 microglobulin excretion greater than 0.5 mcg/min and IgG excretion over 250 mg per day (others use the more sesitive value of 125 mg/24 hours) have both been associated with increased risk of renal progression. (Medline)
Treatment
Treatment recomendations are based on the probability of progression.
Low Risk For patients with a low risk of progressing the recommendation is to stay and pray.
Monitor the creatinine
Institute non-specific antiproteinuric therapy (ACEi, ARB, aldosterone antagonists)
Control the lipids
Tight blood pressure control
Moderate risk
These patient should be initiaed on the Ponticelli or modified Ponticelli protocol. This calls for three consecutive two-month cycles of cytotoxic therapy.
Day 1-3: 1 gram of methylprednisolone. This is usually done as an inpatient.
Day 4-30: Oral prednisone, 0.5 mg/kg daily
Day 31-60: Oral cyclophosphamide 2 mg/kg (chlorambucil in the original Ponticelli)
High risk
Less data is available. Modified Ponticelli maybe appropriate but others recommend cyclosporin.
For patients with resistant disease there is no consensus on what is best and a list of what’s been tried looks like a line up of the usual suspects, nephrology edition.
K/DOQI recommends spending 3-6 months correcting 25-OH vitamin D deficiency prior to graduating to active vitamin D to control secondary hyperparathyroidism in CKD patients. I have been aggressively treating vitamin D deficiency in my CKD clinic for years and have found a pretty modest affect on PTH. Generally you get 20-30% reduction in PTH by correcting 25-OH D but occasionally you get a real responder.
I just saw a patient with modest stage 3 CKD. When I first saw her she had a 25-OH D of 7 and a PTH of 288. I started her on 50,000 units of ergocalciferol a week. It took 12 months but we finally corrected her vitamin D deficiency and her secondary hyperparathyroidism just melted away.
