Pregnancy outcomes in recovered AKI
In a study of 105 pregnancies classified as rAKI (pregnant women with history of recovered AKI) were compared with 24640 control pregnancies-authors noted that “past episode of AKI, despite return to normal renal function before pregnancy, associated with meternal adverse outcomes in pregnancy”. Women with r-AKI were more likely to have preterm deliveries and deliveries by cesarean section compared with women without AKI (40% versus 27%; P=0.02). Also rAKI were more likely to have -preeclampsia, preterm preeclampsia, and early preterm preeclampsia (23%, 10%, and 7% versus 4%, 1%, and 0.4%; P<0.001). In offspring of mothers with r-AKI, 40% developed the composite adverse fetal outcome (preterm delivery, NICU admission, small for gestational age, or perinatal death) versus 19% in those without AKI (P<0.001).
Clear message is -monitor young women with rAKI for maternal and fetal complications if they get pregnant. Don’t jump to the conclusion and blame past AKI for these complications though! Unlike other AKI outcome literature claiming host of bad outcomes associated with AKI in long run, authors of this paper (in addition to acknowledging limitations of retrospective database analyses) make sensible conclusion,”We, therefore, hypothesize that the underlying metabolic milieu (or other shared risk factors) of these women confers risk for both preeclampsia and AKI.”
Hyponatremia: guidelines on guidelines
‘There are only two tragedies of human life…one, not to get what you want and other is to get it’ said Oscar Wilde. Had he been a nephrologist, he would have said,’there are only two tragedies in the management of hyponatremia…one not to correct it and other is to correct it!’
Here and here are two guidelines on hyponatremia (european and american) and this JASN article tries to compile them together. Whatever formula you choose, everyone except serum sodium obeys them. I remember my residency days when more often than not serum sodium would either not change or change very little or change in opposite direction. Algorithms beginning with assessment of volume status can only impress your board examiners as differentiation of euvolemic vs hypovolemic hyponatremia by clinical assessment can just be as accurate as toss of coin [sensitivity (50%–80%) and specificity (30%–50%)].
Only test that works at beside is repeated measurements of serum sodium and urine output trend-sudden onset of polyuria being the harbinger of dangerous overcorrection. In elderly, CKD, and for those on thiazides even urine Na can’t be relied upon.
Some important points:
-Safety limits have consistently decreased over last two decades from 14-16meq per day to 6-7meq per day given the dangers of overcorrection.
-Fractional excretion of uric acid >12% has the highest sensitivity and specificity to diagnose SIAD (i don’t know who does it)
-Coeptin which is one of the degradation products after prohormone is cleaved to form vasopressin and unlike vasopressin is more stable and can be assayed easily. May make our life easier if it becomes commercially available.
-In severely symptomatic acute hyponatremia, both guidelines prefer bolus 3% saline (100-150ml over 10-20min; can be repeated x3 if needed) over infusion (which is prevalent practice).
-Vaptans are NOT for severely symptomatic or acute hyponatremia; moreover if you overcorrect while using vaptans you lose DDAVP as an option to lower back. Urea on the other hand can be safer and effective option (i dont know how to get it)
“If you can measure it, you can associate it with something” and this issue of CJASN is full of such associations which only rarely turn out to be causal. Serum phosphorus and graft loss, TG/HDL ratio and mortality in dialysis, monocyte count and risk of CKD/ESRD, CRP and GFR decline to name a few. Time will be better used reading two nice reviews –IgA nephropathy and SGLT2 inhibition.
SGLT2 inhibitors in addition to glycemic control, have been shown to lower your blood pressure, weight, uric acid, and are the only OHA that showed CV benefit. Also New onset of macroalbuminuria, new onset or worsening of DKD, doubling of serum creatinine and initiation of RRT was less in those treated with SGLT2i. EMPA-REG OUTCOME was funded by Boehringer Ingelheim and Eli Lilly-so lets wait for all of these to be confirmed in more studies.
Another interesting article on symptom management in CKD: role of dialysis deals with an important puzzle that nephrologist face in patients with stage 4-5 CKD. “The interpretation of the literature is challenging, because the symptoms associated with uremia are often vague, difficult to quantify objectively, and difficult to distinguish from symptoms that can be attributed to conditions coexisting with advanced CKD or side effects of medications used to manage these conditions. Patients with stage 4 or 5 CKD are prescribed a mean of eight different medications” This is one of the most symptomatic patient population and whether the given symptom complex will be benefited by dialysis is not always simple question to answer. This is especially so in elderly and frail population with multiple other comorbidities and calls for shared decision making involving patient and their caretakers.
Am J Nephrology
Interesting report of 477 patients from Germany who were identified as having euvolemic hyponatremia while on thiazide therapy. No single test could reliably differentiate SIAD from thiazide induced hyponatremia (TIH). Its commonly believed to be hypovolemic hyponatremia due to saliuresis, but its not the case. Ever wondered why Gitleman’s which is a state akin to chronic thiazide use don’t develop hyponatremia? Polydipsia and impaired urea mediated free water excretion are the main drivers of TIH. So whatever may be the cause, be prompt in preventing/treating cerebral edema due to acute hyponatremia (3% saline) and osmotic damage due overcorrection (free water and/or DDAVP). Accompanying editorial nicely summarises the issue of TIH and practical difficulty in differentiating it from SIAD. Here is an excellent blogpost on use of DDAVP in safe correction of hyponatremia.
Nephrology Dialysis Transplantation
Every clinician who is committed to deliver best available care to his patients should have basic understanding of the research methods to be able to make sense of the ever growing literature. I have found most lectures on research methods by statistician boring and sedating and best way to learn this is to apply/interpret them for articles published in your own specialty. This issue of NDT is devoted to clinical epidemiology and is worth archiving to your desktop. Prediction versus etiology, survival analysis, clinical versus statistical significance, relative versus absolute risk, meta analysis -all of them have examples from nephrology literature that makes it easy to understand the concepts.
Sildenafil for glomerular disease
Erectile dysfunction turning out to be ‘blessing in disguise’ for patients with diabetic kidney disease! Here is a paper and an editorial (which I tried hard to read full). I was so disappointed when I noted that subjects of this experiment were rats and mice. Sildenafil seems to act via same pathways as pioglitazone which was once advertised as antiproteinuric. Abstract starts with this background “PPAR-γ agonists, like pioglitazone, appear antiproteinuric.” and probably even after human studies sildenafil will have the same place (?) as pioglitazone in the treatment of proteinuria. Meanwhile we can watch what happens to UPCR after somebody ‘gets started’ on Viagra.
Tukaram JamaleAssociate ProfessorDepartment of NephrologySeth GS Medical College and KEM hospital,Mumbai, India