Friday, August 20, 2010
Kidney Stone riddle: the answer
He had primary hyperparathyroidism and went for a parathyroidectomy. The recurrent laryngeal nerve was severed during the procedure and that left him unable to speak.
He suffered in silence for 6 months before going for a procedure which pushes the vocal cords on the paralyzed side medially. This allows the normal cord to meet the still paralyzed, but medially displaced cord and phonate.
Thursday, August 19, 2010
Kidney Stone Riddle

My face screwed up as I tried to figure out what the hell he was talking about. His next sentence explained everything.
What happened?
Other hints: his stone were conventional calcium oxalate stones, and he had recurrent stones.
I'll leave the answer later today or tomorrow.
Thursday, June 4, 2009
Online endocrine textbook

Here is the link to the section on kidney stones written by Murray Favus. On my brief overview it looks good.
Being in the textbook business in the era of free online textbooks, UpToDate and wiki's has got to be a world of hurt.
Monday, January 5, 2009
Kidney Stones and Chronic Kidney Disease

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.
Wednesday, September 24, 2008
Melamine Milk Poisoning and Kidney Stones

Nephrology rears its ugly head in the news cycle.
The NYT weighs in.
The top food official resigns. I bet he is happy to get away with a forced resignation compared to Zheng Xiaoyu, former head of the chinese FDA who was executed for corruption following the tainted phamaceutical debacle last year.
The interesting is that the same toxin, melamine, was implicated in the pet food renal failure problem in 2007. At that time, the US FDA provided lots of assurances that malamar is not that toxic. Is this a pediatric issue? In some of the articles following the pet food issue a second compound, cyanuric acid, was implicated in the pathophysiology. I have not read anything about cyanuric acid.
More on this as it develops.
The only data I could find on the concentration of melamine in the milk products comes from this ChinaDaily article.
The highest concentration of melamine was found in Sanlu products. Tests show every kg of Sanlu milk food contains 2.56 g of melamine, which can make milk appear rich in protein in quality tests. The chemical is usually used to make plates, bowls, mugs and sundry other products, but is banned from being used in the food industry.
The other tainted products contain between 0.09 mg to 619 mg of melamine per kg.
During the pet food scare of 2007, there was concern that some of the melamine contaminated pet-food reached live-stock and ended up contaminating the food supply. The FDA estimated the tolerable daily intake of melamine at 0.63 mg/kg.
The point of departure (POD) is the NOAEL of 63 mg/kg/day from the rodent subchronic bioassay. This POD was then divided by two 10-fold safety/uncertainty factors (SF/UF) to account for inter- and intra-species sensitivity, for a total SF/UF of 100. The resulting Tolerable Daily Intake (TDI) is 0.63 mg/kg bw/day. The TDI is defined as the estimated maximum amount of an agent to which individuals in a population may be exposed daily over their lifetimes without an appreciable health risk with respect to the endpoint from which the NOAEL is calculated.
Using the concentrations from the China Daily article and the FDA limits on tolerability a 7 kg baby would need to ingest 1.7 liters of Sanlu milk to exceed this safe limit (of note, at the highest concentration only 7 mL would exceed the safe limit). Either the safety estimate was off or there is an additional compound causing the toxicity.
Google search for melamine