Wednesday, September 10, 2014

Telenephrology: Is this the answer?

Chronic kidney disease (CKD) is a common medical condition, affecting approximately 26 million adults in the U.S. Parallel to the increasing prevalence of CKD, a record number of patients now have end stage renal disease (ESRD). In 2007, 368 544 patients were on dialysis—a striking 54% increase from one decade earlier. Meanwhile, mortality rates for dialysis patients have declined, and approximately 775 000 people are expected to be alive with ESRD in the year 2020.

The nephrologist—a central provider for patients with CKD, ESRD, or kidney transplants—assumes a critical role in addressing the primary care needs of these patients, who tend to require frequent follow-ups. To meet the projected need for nephrologists inthe United States, fellowship programs should have produced an estimated 436new nephrologists each year since 2000. During the past decade, however, the American Board of Internal Medicine (ABIM) only certified an annual average of 382 nephrologists. This is despite the organizations many efforts and initiatives to recruit physicians to the field of nephrology.  If you do the math, the deficit is alarming.

Telemedicine is the practice of medicine using modern communication technologies when the physician and the patient are separated by distance. The modern communication technologies involved are nothing more intimidating than the telephone, e-mail and videoconferencing. Formally defined by the American Telemedicine Association, telemedicine is the use of medical information exchanged from one site to another via electronic communications to improve a patient’s clinical health status. It has been applied to other specialties, particularly neurology, radiology, psychiatry, ophthalmology, and high-risk obstetrics but nephrology has been a slow starter. Indeed, as a specialty, nephrology may be very suitable for this type of medicine. 

Nephrology is a visual and auditory rather than tactile subject – the skill is in recognizing diseases principally from a history, backed up by demonstrating basic physical signs in an examination and established by laboratory tests. So, if nephrologists based in urban centers can deal with renal patients in distant parts of the country, or even different countries, by means of communication technology, then the problem of reduced access to specialist care may be lessened, if not solved.

Post By Judy K. Tan MD
Mount Sinai Medical Center, New York, New York

Tuesday, September 9, 2014

Twice weekly, three times weekly or daily dialysis- where do we stand?

While observational trials had shown that there is much more benefit in daily dialysis (improved phos control, better HTN control, anemia), the FHN trial in NEJM proved some of the hunch that more dialysis was better in terms of cardiac remodeling and quality of life. This study compared in center patients to standard HD vs daily dialysis.  These were prevalent patients and not incident patients with some residual renal function.  
A recent editorial in AJKD sheds some light on residual renal function as an important predictor of renal survival.  The authors suggest that thrice weekly might rapidly decline renal function compared to perhaps twice a weekly dialysis sessions. But does that matter compared to cardiac outcomes.  The second FHN trial in Kidney international showed that the more intensive nocturnal HD group failed to show benefit compared to the three times a week dialysis.  Interestingly, this was in all incident patients with residual renal function.  The study found that the more intensive HD group lost residual renal function faster and in addition no difference in cardiac remodeling and quality of life. More vascular interventions were also performed in the more intensive arm. 
Finally, the most recent AJN article published this week, a single center study from China shows that twice a week HD preserves residual renal function.  They examined 85 HD patients; 30 of them were initiated with twice-weekly HD for 6 months or longer and 55 patients were started and maintained on thrice-weekly HD treatment. Then a subcohort study in 48 incident HD patients was implemented to assess the independent risk factors responsible for RKF decline during the first year of HD therapy. Clinical outcomes were the same in both groups. The multivariate analysis showed that factors such as the male gender, HD frequency, URR and intradialytic hypotension episode were associated with residual renal function loss. This study’s main outcome was residual renal function and not mortality.  It will be interesting to see and follow these patients to see the mortality data regarding this.

What does this lead us to believe? One size DOES NOT fit all. Perhaps initially, HD should be catered to preserving residual renal function and start slowly. Some patients might require twice a week HD, some three times a week and some perhaps more such as 4-6 times a week.  Should we be doing HD just as we do PD? When we calculate PD related CRCL, we use the residual renal function clearance and then the peritoneal clearance and add them to get to our expected/desired kt/v.  Why shouldn’t we do that in HD as well?  Incident patients might benefit from less intensive HD and prevalent patients who have lost residual renal function, might benefit from more intensive HD.  More studies are needed to answer these questions that the FHN and other studies have raise. 

Tuesday, September 2, 2014

Friday, August 29, 2014

In the NEWS: LCDD without proteinuria: A challenge for nephrologist

Classically Light chain deposition disease(LCDD) presents with proteinuria ( almost in the nephrotic range). A recent article in NDT looks at a small cohort of patients that presented with LCDD with <0.5gm of proteinuria.  They present 14 cases, average proteinuria was 0.3g/day. Most had CKD at baseline.  IgG kappa was the most common light chain followed by IgM kappa.  Only 3 patients had diagnostic myeloma, 2 had WM.  Interestingly 5 had MGUS and 4 had smoldering myeloma.  Serum creatinine decreased in most cases after chemotherapy was introduced. Proteinuria never became nephrotic range.   This is thus far the largest series of such LCDD without proteinuria. Early identification of this atypical variant of LCDD is important.  It seems also that it’s a smoldering form just like the hematologic counterpart and most of these patients had either MGUS or SM and not full blown MM.  

What did the pathology show?-  diffuse tubular basement membrane thickening; some with duplication.  Rare casts were noted.  Nodular sclerosis of GN lesions only in 2 cases and others did have some mesangial hypertrophy and ischemic lesions.  No amyloidosis was noted in any cases. 

Classically thought to be a proteinuric variant of myeloma, LCDD can also present as a non proteinuric disease mainly involving tubules. 

Saturday, August 23, 2014

Ipilimumab and renal disease

Ipilimumab is a human monoclonal antibody that targets T lymphocytes antigen-4 or CTLA-4 and it’s used in clinical practice to treat melanoma.  Does this agent lead to nephrotoxicity?

Where do we encounter CTLA-4 in the renal literature?

Agonists to reduce immune activity using CTLA-4 Ig are available such as Orencia( abatacept) for SLE and RA.  Belatacept is a similar agent used in transplantation literature for treatment and prevention of rejection.  How are they different from ipilimumab that is used to treat cancer?  This antibody binds to human CD152 and enhances T cell response especially against tumor cells. It basically boosts the immune response against the tumor cells.  So invitation of the T cells into the kidney could be possible- and renal injury a potential side effect.

Literature search revealed three published cases.
And a NEJM case report on the drug causing lupus like nephritis.

It seems that the treatment of this leads to activation of T cells that can stimulate a classic vasculitis or interstitial nephritis. 

As the cancer literature grows,  we have to be mindful of the nephrotoxicites of such agents.

Tuesday, August 19, 2014

Concept Map: Thrombotic microangiopathies

This is based on a recent review by George and Nester in NEJM on TMA syndromes. Looking and classifying TMA in this format is much more pathophysiologic than using terms such as HUS and TTP

Out with HUS and TTP and let's use more CAUSE based TMA as the term to help understand pathophysiology and then use the appropriate treatment

**( complement mediated TMA) is a better term then using atypical HUS as it gives more information regarding pathophysiology and not confuse us.

Click on the image for a larger/readable view.

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