You are on page 1of 4

Review points :

Cr: neither filtered , nor reabsorbed/metabolized


Estimate of clearance so estimate of flow-filtration = GFR
Derived from MSK/Food = produced at a constant rate !

GFR: can not be measured directly so filtration Markers used to estimate


e.g INULIN =freely filtered at the glomerulus, and is neither secreted, reabsorbed, synthesized,
nor metabolized by the kidney
estimate: GFR x SCr = constant
Key : GFR falls , Cr excretion stops = retention until doubles then filtered load equals
excretion.

e.g GFR drops by 50% , Cr retention until doubles original serum value =filtered load
reached =now excretion is equal.

! mild kidney dx : small rise in Cr = sudden fall in GFR


! advanced kidney dx: sudden rise in Cr = reflects absolute reduction in GFR its
worse

Rules :

Rise in Cr =GFR drop


Drugs : decrease secretion =compete for OAT = TMP SMX , H2 blockers ,
How come ? organic cation in the physiologic pH range and is secreted by the organic cation
secretory pump that can be inhibited by other organic cations.

BUN/GFR
varies inversely with the GFR
not helpful because independently changes despite GFR level
urea production not constant , ? = MSK break down , trauma , steroids , liver diseae,low
protein diet .

key : liver disease=near normal BUN/SCr but still could have drop in GFR

most accurate test : Cystatin C in combination with creatinine is more accurate for the
assessment of GFR than serum creatinine in certain populations and can be used as a
confirmatory test for diagnosis of CKD and for estimation of GFR
CKD

Definition

Damage for > 3 mths


Urine albumin excretion > 30mg/day or equivlant
GFR <60ml/min
abnormal blood tests

ESRD
GFR <15ml/min or need for dialysis

Clues :

Protienuria , hematuria , cellular casts

Work up
U/A = analysis , proteins , microalbuminuria , creatine clearance ( looking for tract
disorders)
Serum Cr
GFR
BUN
Albumin
Cystain c = all cells produce it kidneys regulate it = to high = Kidney damage
Measure PTH

Imaging
U/S = looking for abnormalities , size /position
Ct scan =structural problems or presence of obstruction
Biopsy
Identify specific disease
Evaluate extent of damage
Find out why a transplant may not be doing well
Reversible causes of renal failure

Decreased renal perfusion


Moa: hypovolemia from vomiting , diarrhea , diuretic use , bleeding, NSAIDS,ACE
Patho: Fena <1 =urine NA less then <25
Nephrotoxic drugs
Moa : contrast media especially in DM , aminoglycosides =(culprits=gentamycin,!!!)
=tubular damage =ATN
Hyperkalemia= excretion normal as long as aldosterone/ distal flow are good
Mineral bone disease= hyperphosphatemia=secondary hyperphosphatemia=more ca2+ =
vascular calcification
HTN
Anemia =low epo
Volume overload: Dietary restriction of NA + diureics
Uremic bleeding =check PLT, echo pericaditis, CT head for AMS r/o stroke

Risks = CAD
Traditional =hypertension, smoking, diabetes, dyslipidemia, and older age
Nontraditional =uremic toxins, anemia, elevated levels of certain cytokines, an increased
calcium load, abnormalities in bone mineral metabolism, and/or an increased
inflammatory-poor nutrition state.

Management

Tx reversible causes = toxic drugs, decreased perfusion , obstruction


Prevent/slow progression of renal disease
Tx of complications of renal failure
Adjust drug doses
Prep for dialysis

Tests to consider for certain pathologies in CKD

Serum and urine protein electrophoresis


Serum urine free light chain
Screen monoclonal proteins
ANA, DsDNA
Complement =Glomurulonephritis could be depressed !!
C-ANCA, P-ANCA
HEP B , HEP C
Imaging , U/S,

Indications for renal dialysis


Pericarditis or pleuritis (urgent indication).
Progressive uremic encephalopathy or neuropathy, with signs such as confusion, asterixis,
myoclonus, wrist or foot drop, or, in severe, cases, seizures (urgent indication).
A clinically significant bleeding diathesis attributable to uremia (urgent indication).
Fluid overload refractory to diuretics.
Hypertension poorly responsive to antihypertensive medications.
Persistent metabolic disturbances that are refractory to medical therapy. These include
hyperkalemia, hyponatremia, metabolic acidosis, hypercalcemia, hypocalcemia, and
hyperphosphatemia.
Persistent nausea and vomiting.
Evidence of malnutrition

You might also like