musings of a salt whisperer
I have two patients who routinely have significantly lower spot protein to creatinine ratios as compared to 24-hour urine for protein.
The urine electropheresis shows non-specific proteinuria.
Any ideas? What am I missing?
We have come to that time once again. Time to interview a gaggle of highly qualified candidates for a few spots in our nephro fellowship. Here is is how it looks by the numbers:
The number of new nephrologists is just under 400 per year.
30% are woman and 51% are US medical graduates. This is a decrease in the number of foreign medical grads from 50% in 1999 to 40% in 2005.
757 applicants applied for 372 spots in at 135 accredited programs in 2007.
Nephrology is the fourth most popular internal medicine sub-specialty after cards, Heme/Onc and Pulmonary/Critical care (look at the bottom of the list and add that to the combined Pulm/Crit Care).
42 kidney transplant programs are available.
There are 19 programs in interventional nephrology however, only 6 are certified by the American Society of Diagnostic and Interventional Neophrology (ASDIN).
VADT is yet another negative trial showing a lack of benefit from controlling blood sugars.
That makes three negative trials in the last 12 months.
All three of these trials were looking to prove that better glycemic control could reduce strokes and heart attacks. We have known since the early nineties that good glycemic control prevents or delays microvascualr complications (kidney disease, blindness, neuropathy) but the data on cardiovascular disease was lacking. This is important because relatively few diabetics develop ESRD and most patients die of heart disease, a macrovascular complication. For example in type 1 diabetics the 20 year risk of developing ESRD is only 2.2%, while the risk of death is four times that at around 10%.
Unfortunately, this looks like a bust. Not one of the trials have shown any sign that improved glycemic control translates into reduced heart attacks or strokes.
Here is a powerpoint lecture on DM I gave a year ago. SlideShare kind of butchers the formatting so if you are really interested download it rather than whatch in the online viewer.
My list (with help from my partners and fellows) of the Top Nephrology Stories of 2008
Top unique keywords that lead people to this blog:
Top blog entries by traffic
One of the important studies released at Renal Week 2008 was the ASTRAL Trial (Angioplasty and STent for Renal Artery Lesions). This is the largest trial ever done on renal angioplasty. This seems like one my constant battles with cardiologists. I get a consult a month regarding whether patients should get a renal agioplasty done. I am almost always fighting against this based on prior information which showed marginal improvements in blood pressure control with the therapy and no change in the level of kidney function. However this data was questionable due to a high cross-over rate (i.e. 22 of the 28 patients initially randomized to drug therapy alone underwent angioplasty after 3 months).
This shows that the 806 patients randomized to ASTRAL dwarves all of the previous work on the subject. (source)
ASTRAL was billed as the definitive study to determine if angioplasty and stent preserved renal function, improved blood pressure, prevented hospitalizations, or reduced CV mortality. Patients were followed for 27 months. The enrolled cohort is representative of that are typical candidates for renal revascularization. Here are the graphs from the Investigator Newsletter:
GFR
The bulk of patients had moderately severe renal disease. It is important that they did not select patients too late in the disease where revascularization may be too late to save the kidney. Similarly you wouldn’t wat to intervene too early where the splay between the groups may take longer than 27 months to materialize.
The average GFR was 40 mL/min.
Of note: if you just looked at patients with an initial GFR<25, size="4">Length
The fact that the affected kidney size was pretty good goes against the potential criticism that they were revascularizing too late after permanent infarction and scarring has ocured.
Stenosis
Most of the patients had severe stenosis, a high grade that if found during a diagnostic angiogram would be followed by an intervention.
Results:
At follow-up, no difference in creatinine, blood pressure, time to first renal event, or mortality (p = ns for all outcomes)
The authors emphasized that there was no benefit for the entire cohort but they feel that the therapy is likely helpful for some subset of the population. I agree, like every nephrologist, I have seen patients have dramatic improvements in renal function following angioplasty for RAS. With the immense ASTRAL database it will be exciting to see if the authors can tease out which subgroups benefit from this technology.
Despite having seen multiple patients benefit from renal artery angioplasty I have remained a skeptic of the technology. Part of this comes from the older flawed and small trials and partly due to the ineffectiveness of cardiac angioplasty to help patients except in regards to reducing angina (a condition that doesn’t have a renal analog) or in patients having an active infarct.
One of the biggest stories coming out of Renal Week 2008 was this abstract which linked kidney stones to the development of CKD. This is an important study but I filed it under “no duh.” Patients with kidney stones tend to be heavier, have more hypertension, get episodes of acute renal failure and have repeated instrumentation on the kidneys. They also have gout, and associated hyperuricemia, an increasingly important progression factor for CKD and hypertension.
The most important aspect of this is the question that was left unanswered: do kidney stones cause CKD. The association makes sence but causality would be much more important because we have good tools to prevent kidney stones and it would be wonderful if by preventing kidney stones we could also be preventing future kidney failure.
Hopefully this question will be answered in the near future.
[F-FC202] Kidney Stones Are Associated with an Increased Risk of Developing Chronic Kidney Disease
Andrew Rule, Eric Bergstralh, L. Joseph Melton, Xujian Li, Amy Weaver, John Lieske Nephrology, Mayo Clinic; Health Sciences Research, Mayo Clinic
Background: Kidney stones lead to chronic kidney disease (CKD) in patients with rare genetic diseases (e.g., primary hyperoxaluria), but it is less clear if kidney stones are an important risk factor for CKD in the general population.
Methods: A cohort of all Olmsted County, MN residents with incident kidney stones in the years 1984-2003 were matched 3:1 to controls in the general population based on index date (first stone diagnosis for stone formers and any clinic visit for controls), age, and sex. Diagnostic codes (yrs: 1935-2007) and serum creatinine levels (yrs: 1983-2006) were captured with the linkage infrastructure of the Rochester Epidemiology Project. Risk of incident chronic kidney disease was assessed using clinical diagnostic codes, end-stage renal disease (dialysis, transplant or death with CKD), sustained (>90 days) elevated serum creatinine (>1.3 mg/dl in men, >1.1 mg/dl in women), and sustained estimated glomerular filtration rate (eGFR) < 60 ml/min/1.73 m2. Proportional hazards models adjusted for age, sex, and baseline and time-dependent co-morbidities (diabetes, obesity, gout, hypertension, hyperlipidemia, alcohol, tobacco, coronary artery disease, heart failure, cerebral infarct, and peripheral vascular disease).
Results: After excluding persons with prevalent CKD, 4424 stone formers and 10995 controls were identified with a mean follow-up of 8.4 and 8.8 years, respectively. Stone formers had an increased risk of developing a clinical diagnosis of CKD [hazard ratio (HR)=1.6, 95% CI: 1.4-1.8, see figure], end-stage renal disease (HR=1.4, 95% CI: 0.9-2.2), a sustained elevated serum creatinine (HR = 1.4, 95% CI: 1.2-1.7), and a sustained reduced eGFR (HR = 1.4, 95% CI: 1.2-1.6).
Conclusions: These data argue kidney stones to be an important risk factor for chronic kidney disease.