Nephrology
Clinical discussions on kidney disease management, dialysis, transplantation, and electrolyte disorders.
Recent Discussions
Do you routinely check a TSH level in patients with recurrent kidney stones who have hypercalciuria of unknown cause?
No. Although hyperthyroidism is a reported cause of hypercalcemia and hypercalciuria, it must be very rare cause of nephrolithiasis. I suspect the patient would be obviously hyperthyroid on examination. Hyperparathyroidism is a much more common cause of kidney stones. In my practice, if the stone an...
What is your plasma oxalate target when treating patients with lumasiran for end stage kidney disease secondary to primary hyperoxaluria type 1?
We have a lot of experience with the PH1 population on dialysis here using the Mayo Clinic Laboratory Plasma oxalate assay. Ideally, we shoot for a pre-dialysis value of 30 or less. In our experience with this and other Hyperoxaluric patients, the risk of oxalosis would be low at those numbers and a...
What is your approach to recurrent uric acid stone formers who have a persistently acidic urine pH and are unable to tolerate potassium citrate?
I use sodium bicarbonate. I teach the patient how to titrate the dose using pH dipsticks to get the urine pH >6.0. Although sodium may increase urine calcium excretion, in uric acid stone formers, this is not an issue. Long experience with sodium bicarbonate tells us it does not raise blood pressure...
Do you avoid ESAs in patients with end stage kidney disease who also have heart failure due to increased risk of stroke?
If the question is whether I avoid ESAs in patients with ESKD who also have heart failure, the answer is no for several reasons. The warning in the ESA package insert regarding using ESAs with caution in patients with heart failure (HF) comes from the CHOIR study (Singh, et al., PMID 17108343) of no...
Do you give a short-acting antihypertensive before starting outpatient hemodialysis on an asymptomatic ESKD patient with a predialysis blood pressure of more than 200/100?
I rarely use short-acting antihypertensive agents. I usually give long-acting calcium channel blockers, b-blockers or ace inhibitors if the blood pressure is very high. Ultimately the best option would be to remove more and more fluid slowly over time if patient can tolerate it. However, I find flui...
What is your approach to management of recurrent nephrolithiasis in patients with mixed composition uric acid and calcium phosphate stones?
Likely the urine pH is more typically low in such patients, since the uric acid components will dissolve during periods of higher pH. Consequently, the appearance of uric acid crystals in the stone suggests that the urine pH is more typically low. Drinking more fluid to cause more dilute urine alway...
Are there patients with recurrent nephrolithiasis for who you recommend magnesium supplementation to reduce stone risk?
While magnesium supplementation may be justified on theoretical grounds, I have never used magnesium supplements as a treatment exclusively for kidney stones. I have only ever seen or used magnesium supplementation in stone patients that had concurrent hypomagnesemia.
What is the current recommendation for using thiazide diuretics in patients with calcium oxalate stone disease, given the negative results of the NOSTONE trial?
This trial will have no effect on my practice. Seven of 10 previous studies of thiazides for stones were positive, as was a meta-analysis. My preference is for the longer-acting drugs indapamide and chlorthalidone; I haven't used HCTZ which is probably a twice-a-day drug, for some years. Note that t...
Do you recommend taking any unique approaches to managing patients with persistent hypertension following bilateral renal artery stenting?
Yes, I will be more aggressive with lipid management, sometimes using PCSK9-INH in addition to a statin, if the cause of the renal artery stenosis was atherosclerotic-related. Also, I typically get yearly ultrasounds to evaluate the patency of the renal artery stents. From a management perspective, ...
What are your next steps when managing patients with suspected Gitelman syndrome for whom genetic testing reveals variants of uncertain significance or novel mutations not well characterized?
If the patient had a clinical syndrome that fit the Gitelman phenotype I would totally treating as such.