- 24-hour urine creatinine was 3,232 mg
- 24-hour urine protein was below the level of detection (<183>
- His CrCl is 102 mL/min
- Advanced Stage 3b CKD by MDRD
- Normal kidney function by 24-hour urine collection
The New England Journal of Medicine this week did a Perspective piece on Melamine. Its amazing to me how a health crisis this big has been essentially ignored up to now by the core medical journals.
The article is in depth and insightful. It suggests, as my former fellow did, that the combination of both melamine and cyanuric acid produced the latest epidemic.
The article continues the obscurity and confusion that comes from mixing parts per million and mg per kilogram.
Since there are insufficient data from humans, the WHO meeting recommended a tolerable daily intake (TDI) of 0.2 milligrams per kilogram of body weight for melamine and 1.5 milligrams per kilogram of body weight for cyanuric acid. The executive summary stated that the TDI is “applicable to the whole population, including infants.” However, exposure to both melamine and cyanuric acid may confer a higher risk, and there are unknowns about long-term renal and other risks. The current limit set by the FDA for melamine in food is 2.5 parts per million, calculated on the basis of ingestion by a person weighing 60 kg.
The dietary exposure based on the consumption of melamine-adulterated infant formula in China at the median levels of melamine reported in the most contaminated brand was estimated to range from 8.6 to 23.4 mg/kg body weight per day, based on data provided by the Chinese Center for Disease Control and Prevention.
I went to an afternoon of lectures at ASN on Klotho and its relationship to calcium. I thought they talked about klotho being involved with proximal tubule transcellular calcium reabsorption via TRPV5/6 but after posting a comment about that here, I find that my memory failed me.
These findings revealed a comprehensive regulatory scheme of mineral homeostasis that is illustrated by the mutually regulated positive/negative feedback actions of alpha-Klotho, FGF23, PTH and 1,25 (OH) Vitamin D. In this regard, alpha-Klotho and FGF23 might play pivotal roles in mineral metabolism as regulators that integrate calcium and phosphate homeostasis, although this concept requires further verification in the light of related findings. Here, the unveiling of the molecular functions of alpha-Klothootho and FGF23 has recently given new insight into the field of calcium and phosphate homeostasis. Unveiled molecular functions of alpha-Klotho and FGF23 provided answers for several important questions regarding the mechanisms of calcium and phosphate homeostasis that remained to be solved, such as :
However, several critical questions still remain to be solved. So far reported,alpha-Klotho binds to Na, K-ATPase, FGF receptors and FGF23, and alpha-Klotho hydrolyzes the sugar moieties of TRPV5. Does alpha-Klotho recognize these proteins directly or indirectly?Is there any common mechanism?How can we reconcile such diverse functions of alpha-Klotho?What is the Ca sensor machinery and how can we isolate it?How do hypervitaminosis D and the subsequently altered mineral-ion balance lead to the multiple phenotypes?What is the phosphate sensor machinery and how can we isolate it? How does the Fgf23/alpha-Klotho system regulate phosphorus homeostasis? How are serum concentrations of Ca and phosphate mutually regulated?
I did a lecture at Providence last week.
I was scheduled to just give a electrolyte lecture without any further guidance. I pulled out two interesting cases I had seen in the last few weeks. Both patients have a non-anion gap metabolic acidosis, but one is hypokalemic and the other is hyperkalemic.
Here is the native Powerpoint files for you to use or edit.
Here is the SlideShare for online viewing
Sat December 13
Thursday through Sunday December 25-28
I was consulted on a patient with acute renal failure and severe acidosis without an obvious source. The intensivist postulated this could be propofol induced B-type lactic acidosis. I had not previously encountered this entity.
Apparently propofol can block the electron transport train of the mitochondria causing lactic acidosis. Clinically the patients present with lactic acidosis, rhabdomyolysis and acute renal failure.
Interesting article showing propofol decreasing oxygen utilization in animal model
Pediatric case in which the doctors captured increased levels of various types of carnitine indicative of altered mitochondrial oxygen utilization.
Craven et al found 24% rate of unexplained metabolic acidosis with propofol use, suggesting a much more common mild form of the disease.
My patient was exposed to only a single dose of propofol so I am skeptical but the lack of an alternative compelling etiology is leaving me considering this disease.
What over the counter medications should I be careful about with my kidney disease?
All over-the-counter medications have the potential to be harmful and so they should only be taken according to the labels and if you have any questions you should call you doctor. However, there are a few over-the-counters that are particularly problematic for patients with weak kidneys. Here they are:
Ibuprofen (Advil, Motrin), Naproxen (Naprosyn). Both of these medications are non-steroidal anti-inflammatory drugs or NSAIDs. There are a number of other NSAIDs that are prescription only including indomethacin, Celebrex and others. The problems with NSAIDs goes for all of these agents, not just the over-the-counter ones. NSAIDs block the production of prostaglandins that trigger inflammation in the body. Unfortunately, in the kidneys, prostaglandins help maintain blood flow. Blocking prostaglandins can decrease the blood flow to the kidney and cause the kidney to shut down. This is more common when patients are also taking diuretics (water pills) and blood pressure medicines called ACE inhibitors or ARBs. (Common ACE inhibitors include Vasotec, Zestril benazapril, Altace or any drug which ends with –pril. Common ARBs include Cozaar, Diovan, and Atacand or any drug which ends with –sartan.)
NSAIDs can also interfere with blood pressure medicines and cause patients to retain fluid.
Sodium phosphorous cathartics. Fleets enemas and oral solutions are used to treat constipation or prepare patients for surgery or colonoscopy. Recently we have learned that these medications can cause severe permanent kidney damage. Little is known about how often this occurs and appears to be rare but people with normal kidney function have developed severe renal failure requiring dialysis or transplant following exposure to these medications. Unfortunately not all doctors are aware of this complication and are still prescribing these medications. A clear picture of who is at risk for this complication has not emerged but experts agree on the following risk factors:
In addition to the risk of damaging the kidneys with sodium phosphorous, patients on dialysis who take these drugs are at risk of severe elevations in phosphorous that may kill them.
Magnesium citrate is sold under the brand names Citro-mag and Citroma. Magnesium citrate is used to treat constipation and to cleanse the bowels before surgery. In patients with severe kidney disease (CKD stage 4 and 5 and dialysis) it can cause harmful levels of magnesium.
Pseudoephedrine is the active ingredient in some cold medicines (Actifed, Sudafed) that are now kept behind the counter due to the fact that pseudoephedrine is one of the ingredients needed to manufacture methamphetamine (crystal meth). Pseudoephedrine raises the blood pressure by about one point and the heart rate by about 2 beats per minute in patients with normal blood pressure or people with well-controlled high blood pressure. This should not cause any problems. However, in patients with poorly controlled or untreated hypertension, pseudoephedrine may cause larger changes in blood pressure and should only be used after speaking with your doctor.
Great bit on refusing dialysis
Tip o’the hat to Stacy without an e
Are MRIs safe for patients with kidney disease?
Sometimes. In 2000 a new skin disease was discovered that caused patients to develop thick skin around their joints, especially the knees. The thickened skin prevented people from bending their legs so they can’t walk. The disease was initially only found in patients on dialysis.The condition was named nephrogenic fibrosing dermopathy or NFD for short.
For a long time doctor’s had no idea what caused NFD. Then in 2006 some doctors in Europe noticed that only patients who received gadolinium during an MRI developed NFD. Other physicians verified this association and now it is generally accepted, though not proven, that gadolinium is at least part of the cause of NFD.
Gadolinium is used as contrast for patients receiving an MRI when doctors want a better view of the blood vessels. It is always used in a related imaging technique called an MRA. The FDA has identified people at risk of developing NFD. The list includes people with:
1. Acute renal failure
2. CKD stages 4 or 5
3. Cirrhosis induced kidney disease (called hepatorenal sndrome)
4. End-stage renal disease on dialysis
There is no proven strategy to prevent NFD except to avoid exposure to this agent. New contrast agents are being developed that do not have gadolinium. If your medical condition absolutely requires a gadolinium MRi then your doctor may schedule special dialysis sessions to remove the toxin right after MRI.
If you are on dialysis or have any of the other risk factors you should make sure your doctor knows about NFD and you should coordinate the MRI with your nephrologist.
There is no risk of NFD if you do not receive contrast with your MRI.
I am writing some patient information articles to go on our SCSP’s website, scsp.net.
I am including them here as I fine tune them. I have been in contact with Dr. Shah, a nephrologist who has produced some gorgeous patient information booklets that we will be posting online also.
I have heard that getting a dye for a cardiac catheterization or CAT scan can damage my kidneys. Is that true?
Yes. X-ray dye is usually made with iodine and is sometimes called iodinated contrast. The dye allows doctors to see the blood vessels and used when using x-rays to diagnose a number of medical problems. The dye that can damage the kidneys is always given intravenously. Another type of dye is given as a oral liquid. This oral contrast is not harmful to the kidneys.
If you have healthy kidneys the IV dye is almost never harmful; however if you have weak kidneys (chronic kidney disease stage 3, 4 or 5) and especially if you also have diabetes or are also over the age of 65 you are at risk of kidney damage from the contrast.
The kidney damage is called radiocontrast nephropathy. The damage is usually temporary (7-10 days) but sometimes it can cause permanent renal failure requiring dialysis.
There are ways to reduce the risk of developing radiocontrast nephropathy, though even in expert haqnds the risk cannot be eliminated. Protective strategies include:
1. Stopping diuretics
2. Hydrating the patient with saline solution
3. Taking an anti-oxidant called N-acetyl cysteine
4. Reducing the dose of contrast
5. Using a contrast agent with less toxicity
It is important, that if you are at risk of radiocontrast nephropathy and are going to get IV contrast that you notify your nephrologist beforehand so she can coordinate the protective strategy to spare your kidneys.