11/5/07njm

**Chronic Kidney Disease: CKD is Part of Primary Care!**

**Moderator: Andy Narva**

**[Case]{.underline}**

53yo male

    DM 2 x ? yrs

            Comorbid conditions:

                        Dyslipidemia

                        PVD, CHF-LVEF 45%

                        Schizophrenia

            Complications:

                        Diabetic retinopathy

                        CKD with nephrotic syndrome

Meds:

Metformin, Insulin, Atorvastatin, Trazodone, Isordil, Metoprolol,
Coumadin, Diltiazem, Furosemide     (ACEI & aldactone stopped recently
because of hyperkalemia 5.5-6)

Smokes 2ppd

\+ Exercise -- runs

BMI 38-41

BP's 130/70-150/100;

Chronic pitting edema

Alc Range 2000-2007    6.0 -- 6.4

  ----------- ----------- ----------- ----------- ----------- -----------
  Date        Creat       BUN         eGFR        Alb/creat   Alb

  8/1/07      1.5         44          52                      

  4/12/07     1.3         23          \>60                    

  4/4/07      1.5         45          52                      

  3/7/07      1.1         20          \>60        2158        3.4
  ----------- ----------- ----------- ----------- ----------- -----------

[Most recent visit:]{.underline}

BP 130/70

Atrial fibrillation

No edema (lost 30# since April)

Alc 12.4

BUN/Creat 52/1.5, eGFR 52, K 4.9

[Questions:]{.underline}\
Should ACEI be abandoned?  What should be the "tolerance" for
hyperkalemia?

Do I need to do anything else to reduce the progression of CKD?

How frequently should Albumin/Creat and other renal function parameters
be monitored?

Once you have reviewed the Clinical Issue below from Dr. Narva, please
let us know your thoughts on these questions on Case #1 (case just
beneath the Clinical Issue)

**[Questions on Case #1:]{.underline}**\
At your Service Unit......

-What should be the "tolerance" for hyperkalemia?

-Do I need to do anything else to reduce the progression of CKD?

-How frequently should Albumin/Creat and other renal function parameters
be monitored?

-Should ACEI be abandoned? 

**Andrew Narva \[narvaa@niddk.nih.gov\]**

**Thu 9/6/2007 1:41 PM**

**Clinical Issue: Clinical usefulness of quantitative urine protein
measurements**

Our providers have serious questions about the clinical usefulness of
quantitative urine protein measurements for diabetics already
identified, and on ACEi¹s, and the time it would take to convince most
of our population to do a quantitative urine protein.  Could you please
supply a more detailed discussion of the rationale and clinical benefits
expected from this GPRA measure?

**Answer from Andy Narva**

I think there is still some confusion about quantitation of proteinuria,
its\' significance and measurement.

Urine albumin determination can be a screening test (determining whether
abnormal albumin excretion {\>30 mg/day which is equivalent to UACR \>
30 mg/g} is present) and as a monitoring test (quantitating albumuria in
a patient known to have \>30 mg/g).  What is new is that we are
encouraging providers to both screen and monitor urine albumin in our
diabetics.

Albuminuria is a continuous risk factor for progressive CKD and CVD
-i.e.300mg is worse than 200 mg is worse than 75 mg.  There is nothing
magic about the 300mg cut-off.  It is simply the lower limit of
sensitivity of the traditional urine dipstick.

Knowing that a person has abnormal albuminuria is important but it is
important also to know the level and whether it is changing.  The KDOQI
Workgroup on Kidney Disease in Diabetes did not endorse albuminuria as a
therapeutic endpoint, not because they didn\'t think it was a likely
useful endpoint, but because long term controlled studies have not been
done utilizing albuminuria as an endpoint.  However it is still
important to know whether a patient who had 400mg/day one year ago now
has 3 grams, or 100mg.

**From the ADA Guidelines:**

\"The role of continued annual microalbumuria assessment after diagnosis
of microalbuminuria and institution of ACE inhibitor or ARB therapy and
blood pressure control is unclear. Most experts, however, recommend
continued surveillance to assess both response to therapy and
progression of disease; suggest that reducing urine microalbuminuria to
the normal or near-normal range may improve renal and cardiovascular
prognosis. This approach has not been formally evaluated in prospective
trials. \"

**From UpToDate:**

\"Recommendations \< We recommend that an albumin-to-creatinine ratio be
measured yearly in patients with type 2 diabetes. In patients with
microalbuminuria, we recommend either an ACE inhibitor or an ARB to
prevent progression of diabetic nephropathy.\"

This issue is discussed in several places in the KDOQI Guideline which I
can forward, if there is interest.

Ideally, a UACR would be done on every diabetic every year.  The
dipsticks which measure albumin only, but at a lower level of
sensitivity than the conventional dipstick, are still semi-quantitative
and not acceptable. The intent of the dipstick which measures both
creatinine and albumin is to approximate a true alb/creat ratio.

For patients who have dipstick positive albuminuria or known to have a
UACR \> 300mg/g, a cheaper alternative for monitoring  is the
protein/creatinine ratio- both urine protein and urine creatinine can be
run on the standard chemistry analyzers in most IHS facilities.

One way to minimize expenditures would be to do a UACR on dipstick
negative diabetics (using the conventional dipstick) and a
protein/creatinine ratio on dipstick positive diabetics.  If you screen
dipstick negative (using the conventional dipstick) diabetics for
microalbuminuria with the microalbumin dipstick (measuring alb and
creat) you should confirm positives with a UACR.

This is an important issue.  Please let me know if you need more
information.

Andy

**Tobe Propst \[TobePropst@semtribe.com\]**

**Tue 9/11/2007 10:09 AM**

I am interested in the questions posed so far about K+ with
ACEI's/ARB's.

As for reducing the progression of CKD, I basically think of it as
primarily a vascular risk issue in the early stages and I believe we
should focus intently on BS, BP, and lipid control, including the
"therapeutic lifestyle changes" (diet, exercise, etc) and appropriate
meds.  I've seen some more recent articles that the "renal diet" is less
important for the earlier CKD stages, and not sure how to advise my
patients in balancing the low fat, low salt, low cholesterol, and
diabetic diet issues, as the different diet recommendations aren't
completely in sync.  My understanding is that goal BP should be about
115/70, a1c \<6.5, and LDL\<70-80 in patients with CKD III or more.  I
make those the priority (and really pushing smoking cessation if they
smoke), which usually takes multiple visits even in highly motivated
patients, and then at later visits I can try to "fine tune" by trying to
get TG's, HDL, etc more optimal, checking ABI's for PVD, etc.  The bone,
parathyroid, volume overload, and acidosis issues generally seem to be
later-stage (CKD IV or V) issues, and I haven't had experience managing
those myself yet.

 

Can someone give a primary care perspective & outline of meaning /
management of....

-other labs used in CKD, ie: Phos, ionized calcium, PTH, vitamin D,
bicarb, etc;

-when/how to appropriately use calcium carbonate, calcitriol, renagel,
nephrovite, sodium bicarb/citrate, etc. 

...and for anemia that appears to be ACD

I'm still in the "look-it-up stage" of when an erythropoietin level is
appropriate, and in epogen & aranesp use.

Also, when a diabetic has proteinuria and perhaps a mildly decrease GFR,
it's generally assumed to be diabetic nephropathy, and as far as I can
tell not much further workup is indicated, but how do we really know
that it's diabetic nephropathy?  I've learned that diabetic nephropathy
is more likely if there is some retinopathy already present, as usually
retinopathy is present before nephropathy; and the proteinuria and
decrease in GFR should be gradual (vs acute renal failure, etc), but are
there others tests that should take place to verify the CKD is from
diabetes? 

Some recommend that a nephrologist should be on board by CKD stage III
no matter what, and earlier in some circumstances.  Is that I.H.S.
policy?

Thank you

**Andrew Narva \[narvaa@NIDDK.NIH.GOV\]**

**Wed 9/12/2007 9:29 AM**

You have a number of questions.  I\'ll answer your last two first.\
\
Your last question concerns **nephrology referral.**  While various
organizations suggest referral at a given stage or GFR, IHS has no
policy on this.  This is appropriate. Rather than focusing on time of
referral, I believe the focus should be on ensuring that the patient
receives the care necessary from an individual who is competent and
interested.  In places where there is a heavy burden of CKD, this may be
a generalist provider.  Sites where there is less kidney disease will
probably have a different threshold for referral because there will be
little opportunity for generalists to develop clinical expertise in more
advanced CKD.  It is important that the patient receives the needed
care, not who provides it.\
\
The key issues in CKD are ensuring that the diagnosis is correct (see
below),implementing appropriate therapy, and monitoring the patient.
 Except for very advanced kidney disease, most of the therapeutic
interventions are very similar to optimal diabetes care as defined by
the IHS standards of care (BP control, lipids, glucose).  The most
important additional interventions are screening for co-morbid
conditions (anemia, malnutrition, disorders of mineral metabolism,etc)
when GFR is less than 60 (obtain Hgb, Ca, Phos,PTH, Alb) and providing
education to the patient on the progressive nature of kidney disease,
the eventual need for renal replacement therapy, and dietary
modification.  None of this requires nephrology referral per se and much
of it may be more effectively accomplished by a provider who has a
longterm relationship with the patient.\
\
A key tenant of the Chronic Care Model (which IHS is committed to
implementing) is integrating specialty expertise and primary care.
 Models for this integration in kidney disease are rare.  IHS, in fact,
has been more innovative than almost any other setting.  One result, for
example, is the very high fistula rate (a quality of care marker) at the
Tuba City dialysis unit.  This rate is not achieved at other Navajo area
dialysis units served by the same dialysis provider and nephrologists
and appears to be due to a system of care implemented by the general
internists and surgeons to educate patients with advanced CKD and
establish vascular access well before the initiation of dialysis.  \
\
It is important to have a collaborative relationship with your
consulting nephrologist.  Their most important role is to assist in
diagnostic problems (e.g.who to biopsy) and therapeutic problems (e.g.
"uncontrollable" HTN, rapidly declining kidney function).  The way in
which the transition in care occurs as  the patient approaches dialysis
will vary from site to site depending on the local IHS staff and the
referring nephrologist.  Most nephrologists are significantly overworked
and, once they understand that the local IHS providers can and will
provide good care to CKD patients, will welcome the help and the chance
to focus on those patients who require management by a nephrologist.  If
the local providers are not addressing the needs of the patients with
CKD and there is a frequent need for emergent initiation of dialysis,
the relationship with the consulting nephrologist is not likely to be as
cordial.\
\
\
Your next to last question involves **appropriate work-up**.  It is
important not to assume that a patient with diabetes and kidney disease
has diabetic kidney disease.  This is especially true for IHS providers.
 If 30-50% of the adults we see have diabetes then 30-50% of the
patients the patients with non-diabetic kidney disease may also have
diabetes.  Generally non-diabetic kidney disease can be ruled out with a
typical history and physical findings  and screening labs.  There have
been no cost-effectiveness studies of screening evaluations but it seems
reasonable to check (after a complete U/A, UACR or P/C ratio, CBC and
renal panel) the following: Hep B and C serologies, ANA, RF, C3,C4
and,in patients over 40, SPEP, UPEP.  Also check: renal ultrasound and
dilated retinal exam.  \
\
If the patient has retinopathy, proteinuria, and negative screening
tests listed above, it is reasonable to assume the diagnosis is diabetic
kidney disease.  Patients who do not conform to these criteria should be
discussed with a nephrologist.  If you do refer the patient, be sure to
send results of the studies listed above along with relevant clinical
information.   A sample "Renal Clinic Referral" form is below.\
\
I hope this is useful.  Will address your other questions another day.\
\
Andy Narva

**Renal Clinic Referral**

**Name**\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
DOB \_\_\_\_/\_\_\_\_/\_\_\_\_
MR#\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

**Reason for Referral:**

***[For diabetics:]{.underline}***

Year of diagnosis\_\_\_\_\_\_\_\_\_\_

Complications: Retinopathy - BDR PDR Not present No dilated exam

Neuropathy PVD Other \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

**[Proteinuria:]{.underline}** Not present Present
since\_\_\_\_\_\_\_\_\_Most recent quantitation Urine P/C\_\_\_\_\_Date

**Creatinines/GFR** \_\_\_\_\_\_\_Date\_\_\_\_\_\_,
\_\_\_\_\_\_\_Date\_\_\_\_\_\_, \_\_\_\_\_\_\_Date\_\_\_\_\_\_,
\_\_\_\_\_\_\_Date\_\_\_\_\_\_

\_\_\_\_\_\_\_Date\_\_\_\_\_\_, \_\_\_\_\_\_\_Date\_\_\_\_\_\_,
\_\_\_\_\_\_\_Date\_\_\_\_\_\_, \_\_\_\_\_\_\_Date\_\_\_\_\_\_

**[Evaluation:]{.underline}**

ANA\_\_\_\_\_\_\_ RF\_\_\_\_\_\_\_\_ C3\_\_\_\_\_\_ C4\_\_\_\_\_\_
HepBSAg\_\_\_\_\_\_ HepC AB\_\_\_\_\_\_

SPEP\_\_\_\_\_\_\_\_\_\_ UPEP\_\_\_\_\_\_\_\_\_

RENAL U/S:

OTHER:

**Current Meds** (or attach list):

**Most Recent Labs:**

**Referred
by**\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**Date**\_\_\_\_/\_\_\_\_/\_\_\_\_

**Contact
Telephone**\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

**Andrew Narva \[narvaa@NIDDK.NIH.GOV\]**

**Wed 9/19/2007 12:05 PM**

Many of the clinical management questions you have asked (nutrition,
bone disease, BP management, etc) were covered in a series of one-page
articles which we published in the IHS Provider from Sept 2002 through
August 2003.  Most of what is in those articles is still useful.  They
are available in the Provider archives located in the Clinical Support
Center part of the IHS website.\
\
Hyperkalemia is a common issue in our patients treated with ACEi and
ARBs.  Diabetics often have hyporeninemic hypoaldosteronism which tends
to raise K.  ACEi and ARBs may further raise the K.\
\
ACEi/ARBs provide significant benefit to our diabetic patients and they
should be maintained on these drugs as long as this can be safely done.
 KDOQI recommends K\> 5.5 as a cutoff to decrease or discontinue these
drugs.  \
\
There are a couple of maneuvers which may lower the potassium and
prolong the safe use these drugs:\
\
1.  Most diabetics require a diuretic as part of their anti-hypertensive
regimen.  Thiazide diuretics are not likely to be effective in patients
with eGFR\<30 (the group most likely to have elevated K); a loop
diuretic (furosemide) is indicated in these patients and should lower
K.\
\
2.  Many of the patients with high K and more advanced disease are also
acidemic.  Correcting the bicarbonate to 22 with NaHCO3 650mg (titrate
dose against bicarb) will lower K.  Use of furosemide to address the
sodium load associated with NaHCO3 will further lower K.\
\
I hope this is useful\
Andy

**Ann Bullock \[ANNBULL@nc-cherokee.com\]**

**Mon 10/8/2007 10:54 AM**

As I mentioned at the beginning of this CKD discussion, we here in
Cherokee have over 350 patients with a GFR \<60.   Our regional
nephrology group is outstanding, but this is obviously way too many
patients for them to handle all the medical issues which arise in this
complex group of patients.  Our policy is to send patients to them for
an initial evaluation when GFR \<60 (or sooner if there is any doubt as
to the etiology of the CKD) and then we co-manage these patients until
they go on dialysis. 

While there are several nationally/internationally recognized documents
on CKD management, we haven't found any succinct, easy-to-follow
treatment guidelines usable by busy clinic providers.  As such, to help
our primary care providers navigate the renal issues they are having to
address, we have created our own CKD treatment algorithm which is now in
final review by both our regional nephrology group as well as Dr.
Narva---once we're sure it is accurate, safe, and agreed upon by our
referral nephrologists, we'll introduce it to our medical staff jointly
with one of our nephrologists.  We are hopeful that this will help all
the providers in Cherokee to test for, identify, and address the
complications of CKD more quickly and effectively.  It used to be that
renal issues at the local level could be handled by a few physicians
with particular interest and experience in this area, but CKD has become
so prevalent that all providers have to be comfortable with at least the
basics.

What are other I/T/U clinics doing to help their providers better
identify and treat CKD complications?

**Graziano, Kristin (TCRHCC) \[Kristin.Graziano@TCHEALTH.ORG\]**

**Mon 10/15/2007 7:46 AM**

Will that algorithm be available for other service units as well?

Thanks, Kristin

**Ann Bullock \[ANNBULL@nc-cherokee.com\]**

**Thu 10/18/2007 12:57 PM**

We would be happy to share our CKD as well as other diabetes treatment
algorithms once they are finalized, which should be shortly.  We'll let
the Primary Care Listserv Discussion group know where they will be
posted once they're available.

As this excellent discussion on CKD winds down, I'd like to thank Dr.
Andrew Narva for sharing his expertise and invite him to summarize the
key points for us as I/T/U providers to take from this on managing our
patients with CKD.