Wednesday, January 30, 2013

New-Onset Diabetes after Transplant (NODAT)

The estimated rates at 12 months posttransplant are 20–50% for kidney transplants, 9–21% for liver transplants, and approximately 20% for lung transplants. NODAT is associated with increased risks of graft rejection, infection, cardiovascular disease, and death. Besides the traditional risk factors for type 2 diabetes (age, family history, obesity, and ethnicity), exposure to immunosuppressive agents often precedes the occurrence of NODAT.

Below are some articles related to NODAT :

Renal Fellow Network: Pearls for Boards

Renal Fellow Network: Pearls for Boards: 1) Surreptitious vomiting or diuretic abuse - metabolic alkalosis, Laxative abuse - non-gap metabolic acidosis . 2)   Aquaporin 2 -  a...

Monday, January 28, 2013

I recently treated the below patient and would like to ask your opinion:

61 year old caucasian male with long standing diabetes-2 on insulin with baseline creatinine of 1.2-1.5 presented with left lower extremity swelling and fever. No h/o diabetic retinopathy. PMH includes CAD s/p CABG, charcots foot with recurrent right lower extremity cellulitis leading to right BKA. Creatinine at the time of this admission was 3.4. Has MRSA bacteremia and left lower extremity osteomyelitis of foot. Treated with daptomycin initially and then changed to lenezolid. Initial evaluation revealed 0.6 grms of proteinuria. Over a period of few days creatinine improved to 1.6. But started to worsen again gradually over next 10 days with peak creatinine of 3.8 and BUN 116. Developed fluid retention leading to pulmonary edema. Has worsening leukocytosis. He was started on Hemodialysis via right IJ tunnelled catheter.

1) What would be the cause of his recurrent AKI?
2) Would you do biopsy?
3) Any other investigations?

Friday, January 25, 2013


27 year old obese lady with CKD 3 with stable creatinine of 1.7 and 1 gm of proteinuria referred to you for opinion regarding her pregnancy.   Her etiology of CKD is FSGS thought to be secondary to obesity.  This is her first pregnancy and She is in her first trimester of pregnancy. She was adviced not to plan pregnancy because of CKD and also because of ARBs(Angiotensin Receptor Blockers). Inspite of the caution she conceived. Her BP is well controlled and physical exam is unremarkable except obesity. What would be your recommendation?

1) Terminate pregnancy.
2) Continue pregnancy as well as ARBs
3) Explain the risks and leave upto the patient to decide.
4) Continue pregnancy but change ARBs to methydopa.

Renal Fellow Network: eJournal Club - Hemodiafiltration

Renal Fellow Network: eJournal Club - Hemodiafiltration: A few years ago, a unit that I worked at started using hemodiafiltration (HDF) routinely for the first time. Prior to starting our patients...

Wednesday, January 23, 2013

Membranous Nephropathy: Treatment in setting of declining renal function

Roughly 1/3rd of patients with membranous nephropathy experience a progressive deterioration in renal function over time.  Thanks to Pradeep for bringing a new RCT from Lancet to our attention, which focuses on this subpopulation of MN with declining renal function.  This trial randomized patients to conservative treatment, cyclosporine x 12 months, or alternating montly chlorabucil/prednisolone.  Patients in the chlorambucil/prednisolone group had a lower risk (hazard ratio 0.44 [0.7-1.95]) of reaching the primary endpoint of a 20% further decline in renal function, as compared to the other two groups.  Notably, the chlorambucil group, but not the cyclosporine group, received steroids. The authors concluded "For the subset of patients with idiopathic membranous nephropathy and deteriorating excretory renal function, 6 months’ therapy with prednisolone and chlorambucil is the treatment approach best supported by our
evidence. Ciclosporin should be avoided in this subset."

Kiran Goli adds: The original ponticelli protocol still holds good and has a very good response rate. Chlorambucil was originally used in the study but most of the physicians use cyclophosphamide since studies revealed similar efficacy with less toxicity (most worrisome is malignancy). Some may choose CNI particularly in young patients with unfinished families for whom fertiility is important...Kiran.

Thursday, January 17, 2013

Loin Pain Hematuria Syndrome

54 year old female presented with 5 month history of B/L flank pain constant with intermttent exacerbations and one UA in past positive for blood, dipstick in office also positive for blood. No evidence of UTI. NSAIDs use on and off. One differential is LPHS.
Attached is a good review article .

Imp points: 
1.Majority of the cases are females but recent reports have higher male population. 
2.Pain episodes may be associated with low-grade fevers and dysuria, although there is no evidence of concurrent urinary tract infection.
3. Lowgrade proteinuria has been reported in some patients, primarily in the setting of an attack of flank pain.
4. Biopsy may show mild tubular atrophy, patchy interstitial fibrosis, glomerulosclerosis, arteriolar hyalinosis, and subcapsular cortical ischemia. Electron microscopy in some patients reveals abnormally thin or thick glomerular basement membranes.
5.In LPHS associated with Thin Basement membrane ACEIs can decrease severity of pain as suggested in this study. 

6.Most importantly, renal biopsy should be considered on all patients in whom the diagnosis of LPHS is considered as 21% patient were found to have immunoglobulin A nephropathy, especially if proteinuria (even tubular proteinuria) or renal dysfunction is present

Tuesday, January 15, 2013

Metformin-associated lactic acidosis

Today we saw a patient in continuity clinic for hospital follow-up who had been hospitalized with severe lactic acidosis (initial pH <6.8, lactate 14.7), shock, and severe acute renal failure. Her medications at the time of admission included metformin. No other cause of the lactic acidosis/shock was found (all cultures negative). She had longstanding DM and HTN, but no history of CKD. She was dialyzed once, and recovered fully.

Metformin-induced metabolic acidosis is a rare but well-characterized complication of metformin therapy, seen in the setting of either acute kidney injury or chronic kidney disease. Metformin is excreted by the kidneys, hence accumulates to toxic levels in the setting of acute or chronic kidney disease, either with chronic use or in acute overdose. Mortality in this condition is high (45%), and lactate levels are not predictive of mortaility. Metformin is thought to induce lactic acidosis via its inhibition of hepatic gluconeogenesis (conversion of lactate and pyruvate to glucose) and via a direct stimulation of lactate production from glucose in the small intestine. Hemodialysis should be considered in the setting of metformin toxicity, especially when renal failure is present.

It should be noted that when used appropriately, large epidemiologic studies have failed to show an increased risk of metabolic acidosis in patients treated with metformin as compared with other diabetic medications, hence it is considered safe.

-SEM 1/11/13
This was a educational case, I found a good review article 
According to FDA prescribing guidelines Metformin is contraindicated for SCr >/=1.4 (women) and >/=1.5 (men) but with these SCr values there can be great variation in eGFR. Canadian, UK and Australian guidelines includes eGFR in addition or in place of SCr values and probably will be better to follow to prevent the use of metformin in people with low renal functions.
Higher metformin concentrations do not consistently occur in those with more severe degrees of lactic acidosis. Metformin levels are not linked to mortality in those who develop lactic acidosis, perhaps reflecting the primary effect of the underlying cause of the acidosis (e.g., hypoxia, hemodynamic compromise) on outcomes rather than incriminating metformin itself. Even with these limitations I think MALA should be a differential and as Dr. Maynard mentioned IHD/CRRT should be considered, especially in patients with renal failure.
Pradeep 1/12/13