TOPIC DISCUSSION: Asymptomatic Hyponatremia

A nice editorial in my favorite journal Nephrology Nature Reviews talks about the " asymptomatic hyponatremia" syndrome.  When we see a calcium > 11 and no symptoms, we admit and treat. When we see a K of >6.0, we treat, so when we see an asymptomatic hyponatremia say of 130, why don't we treat? is what is asked in this editorial. The editorial brings in the points of 30% of elderly population in nursing homes having low Na levels and increase risk of falls and fractures.  The cirrhotics, CHF patients who run in NA 130-135 but are having no symptoms, should they be treated? and with what. With the new agents out now ( V2 receptor antagonists, FWR or lasix) will be the other question?
This has to be further studied and looked at in my opinion.
At least in part, perhaps culprit agents should be discontinued - such as SSRIs, HCTZ to start with
and prevent worsening perhaps of the hyponatremia.
Check out this nice editorial, a must read

IN THE NEWS- RENAL ANGINA SYNDROME

Nephrologists are trying to catch up with the cardiologist. We are in the midst for a search for a troponin for kidney injury and this is important. several markers are being studied but none really validated and ready for clinical use yet.
What do we really need: How can we suspect renal injury early enough to trigger biomarker testing and more aggressive renal monitoring?
They suggest an angina equivalent for kidney injury....
What is that?
Oliguria, fluid overload and small changes in crt being renal angina equivalents. If these occur in an ICU patient, a more aggressive monitoring should be employed: urine chemistries, more frequent crt monitoring, cystatin C testing and perhaps an early renal consultation

CLINICAL CASE 10, ANSWER AND SUMMARY

Fun with numbers.. Na 140 mmol/L K 4.0 mmol/L Cl 110 mmol/L pH 7.0 pCO2 35 mmHg pO2 75 mmHg HCO3 8 mmol/L. What is the disorder?

In this case, we see that the ph is 7.0 suggesting acidosis as a primary disorder and HCO3 is 8 as well suggesting a metabolic acidemia.  

1. Calculate AG= 22

So there is an anion gap metabolic acidosis

2. Then lets do the Winter's formula

which is 3/2 * bicarb +8 +-2 = PC02. In this case, 3/2 *8= 12+ 8= 20. So the PCO2 expected should be 20 but here its 35.  Hmm. so there is more PCO2 production when it should be suggesting a superimposed

Resp acidosis.

3. A delta delta should be performed to make sure there isn't a third disorder.  Change in your AG is 22-12= 10. So your bicarbonate should be 24(normal) -10= 14. But your bicarbonate here is 8, more lower than expected suggesting another significant non gap acidosis.

So this patient has a severe acidosis--> AG+ non gap + respiratory acidosis.

TOPIC DISCUSSION: PHOSPHATE BINDERS

Check out this week's NEJM issue:It has a nice drug review on Oral Phosphate Binders in patients with kidney diseases.
It highlights the history of binders, cost differences and basic characteristics of types of binders
1. Ca based
2. Sevelamer family
3. Mg Based
4. Lanthanum
5. Aluminium based

What was more fascinating is whats under development.
**Fermagate ( a new mg based binder)
**Colestilan ( non metallic anion exchange resin)
**Niacin and Nicotinamide
What is also interesting is the point that patients with advanced kidney diseases have elevated salivary phosphate concentration.  And no matter what they eat, that gets absorbed. A study showed that chewing gum containing a novel chitosan compound was effective in lowering serum phosphate levels and salivary phosphate levels.
http://www.ncbi.nlm.nih.gov/pubmed/19121775
A good review for fellows!

TOPIC DISCUSSION: A rare case of statin induced rhabdomyolysis leading to respiratory failure and hemodialysis

Someone with hypercholesterolemia and chronic lower back pain on simvastatin 80mg develops Rhabdomyolysis. Over next few days, develops progressive ascending weakness and dysphagia limiting oral intake. Muscle weakness was pronounced with proximal emphasis. Respiratory failure ensues and intubation happens.  Peak CPK of 88747 in spite of aggressive hydration and subsequently required hemodialysis. Hepatitis was severe as well. A quadriceps muscle biopsy demonstrated fragments of muscle with fiber loss and dropout, no significant inflammatory changes. Nerve conduction studies showed motor greater than sensory neuropathy affecting both the upper and lower extremities.

Rhabdomyolosis can be dangerous. As we know that statins can cause renal damage and hepatitis but degree of other muscle damage is rare to see. This is an unusual case vignette of both severe rhabdomyolysis with possible diaphragmatic and accessory muscle involvement. Muscle involvement in statin toxicity has typically been skeletal, it is likely that the respiratory muscles had widespread involvement which led to respiratory failure. In general, Patients respond to drug cessation and therapy with steroids or immunosuppressive agents. This case highlights the need to screen patients in the setting of a recently introduced or dose escalated statin therapy especially in the elderly. Severe skeletal myositis should prompt the treating clinician to monitor the respiratory status carefully. Clinicians should also be vigilant for visceral (liver ,kidney) and smooth muscle ( bowel,bladder) involvement. 

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IN THE NEWS: GLOSEN Study

Idiopathic Membranous Nephropathy:- to treat with immunosuppresion or not to treat is the question at hand.
The classic division has been via the Toronto Registry of breaking down in terms of low risk of progression, medium risk and high risk based on degrees of proteinuria.
This landmark paper just published in JASN April issue really questions the need for treatment early on.
This retrospective trial, very large set of patients showed that spontaneous remission (SR) occurred in 30% of patients; but the decline in proteinuria might take up to a year.  What was more interesting is that, despite remission in the low proteinuria group, a significant number in the moderate proteinuria and 22% in the >12gm of proteinuria had SR as well.
This is different than what was previously thought. SR is not very common in patients with >12gm of proteinuria. On the other hand, this study showed the opposite and that significant amount of these patients had a SR.
From the point of a physician deciding when to start immunosuppresion in this high risk category., this study might shed some more light.  Four features that defined early remission were female gender, lower proteinuria, lower serum crt and treatment with ACEI/ARB.
What this study might teach us is that:- Perhaps the first 6-9 months is a wait and watch period for that high risk >12gm group. If there is a decline by 50% in proteinuria, perhaps a SR is coming on and not to initiate immunosuppresive therapy; just continue anti proteinuria regimen like ACEI/ARB.  If in those 6 months, proteinuria doesn't improve and other complications of nephrotic syndrome ensue, renal function is declining, immunosuppresive therapy might be needed.
A nice editorial is also a good read with this study. Keep in mind its still a retrospective study, but might give some answers that we didn't have for a long time.

IN THE NEWS: Dialysis Time

Interesting article in Kidney Internationa looking dialysis time (in-center, thrice weekly) comparing standard 4hours to shorter treatment and looking at outcomes. They found that patients with shorter treatment times had higher all cause mortality at 1 year, and this was a potentially independent variable.

The study design was observational in nature, looking at session length as a time varying exposure (rather than just baseline), and looking at only incident patients. Finally they analyzed the data to adjust for time varying confounders.

The article also suggests reasons as to why this might be (all reasons we would expect). Although recent studies suggest more dialysis does not translate to significant clinical outcomes in the setting of AKI, chronic dialysis seems to benefit from more dialysis (e.g. nocturnal dialysis)