Tag: kidney stones

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Unintended consequences: Oxalate nephropathy and bariatric surgery.

Near the end of Swapnil’s sweeping summaries of the renal denervation articles for this week’s NephJC, he discussed safety. In the trials, the procedure was remarkably safe but Swap brought up possible future consequences. These are adverse events that could never be measured in a real-world trial:

Renal denervation is permanent. Blood pressure medications can be stopped. Why does this matter? Maybe if a patient subsequently develops sepsis or hypovolemia? The sympathetic system exists for a reason….See this case report. In this study of sheep with CKD, bleeding caused a much more severe drop in blood pressure.

This reminds me of bariatric surgery. We had been doing Roux-en-Y for weight loss for decades (See meta-analysis) when, in 2005, Nelson published a case series of calcium oxalate stones, including a couple of cases of ESKD with dialysis dependence due to oxalate nephropathy. Their work was backed-up in this report.

A massive meta-analysis ofover 700(!) studies of weight loss surgery from 1990 through 2002.

Oxalate nephropathy is secondary to increased oxalate absorption following the Roux-en-Y procedure. There are two theories as to why this is:

  1. Fat malabsorption, one of the goals of the therapy leads to saponification of intestinal calcium. Since calcium is unavailable to bind and trap oxalate in the gut more is available for passive and active oxalate absorption in the distal ilium.
  2. Decreased bile acid reabsorption in the gut leads to unconjugated bile salts damaging the luminal membrane and increased passive oxalate absorption.

Additionally the malabsorption leads to diarrhea and metabolic acidosis. This decreases urine pH and lowers urinary citrate both of which promote calcium oxalate stones. There is also a decrease in urine volume of about 0.5 liters, further increasing the stone tendency of these patients. Dr. Park defined a lot of this in a prospective study of 24-urines after Roux-en-Y.

I have seen patients with ESKD from Roux-en-Y. It is horrible. Since the primary pathology has not ceased, these patients are at risk for the same oxalate nephropathy following a transplant, making a transplant a risky procedure.

Though oxalate nephropathy after Roux-en-Y does occur, obesity itself is a risk factor for ESKD and bariatric weight loss appears to protect patients from this.

From Chang et al. Kidney International Reports 2017 2(2): 261-270. (Another good reference on ESKD risk after bariatric surgery)

This good news tempered with the risk of disaster makes the decision to go for bariatric surgery a bit more nuanced than it is often portrayed. Does renal denervation have similar future land mines just waiting to be exploded in the future? We have no idea what unexpected horrors from renal denervation lie undiscovered.

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#KidneyCON Fluid, Electrolyte, and Acid-Base Workshop

David Goldfarb (@weddellite) and I put on a fluid, electrolyte and acid-base variety show at KidneyCON. The itinerary:

  1. IV fluid taste test
  2. Hypernatremia
  3. Management of calcium phosphate stones: to K-Citrate or not?
  4. Management of chronic hyponatremia, use of DDAVP
  5. Aspirin toxicity
  6. Hyperkalemia

Both of us had a bunch of additional cases that we didn’t get to so be sure to go deep into the presentation files.

Here are the presentation files:

 

 

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Kidney Stone riddle: the answer

The commenters nailed it.

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.

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Kidney Stone Riddle

I was at my great aunt’s 90th birthday party on Tuesday and was chatting with a neighbor. He mentioned that after being treated for kidney stones he couldn’t speak for 6 months.

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.

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Online endocrine textbook

This looks pretty cool.

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.

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Kidney Stones and Chronic Kidney Disease

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.

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Melamine Milk Poisoning and Kidney Stones


Nephrology rears its ugly head in the news cycle.

The NYT weighs in. China Says Complaints About Milk Began in 2007

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