Terms in this set (159)

-A similar relationship exists between BUN and GFR
-As urea is primarily excreted via glomerular filtration, changes in the GFR can change plasma urea levels.
-However, this, too, is not linear - the GFR must be significantly reduced to result in an increase BUN as urea excretion not determined solely by glomerular filtration (Up to 50% of filtered urea is normally reabsorbed from the tubules, passively following water and sodium).
-BUN alone is not a reliable indicator of changes in the GFR
-Urea production not always constant (formed by hepatic metabolism of amino acids - BUN increases with increased hepatic metabolism of amino acids) Can occur with dietary changes (e.g., increased protein intake), greater tissue breakdown (e.g., trauma), and medication use leading to decreased protein synthesis (e.g., tetracyclines).
-GFR THE BEST OVERALL index of kidney FX!!!!!!!!!!!!!!!!!!
-estimating equations for the GFR incorporate association w/ age, sex, race, and body size as surrogates fro creatinine generation.
-Estimating equations: 4 variable original MDRD Study equation
-"re-expressed" MDRD Study equation for standardized serum CR
- COCKROFT-GAULT equation
-CKD-EPI ( chronic kidney disease epidemiology collaberation ; MDRD = modification of diet in renal disease
-GFR equation calculators are available
-many labs regularly report eGFR when CR is ordered
- Calculate eGFR in order to determine CKD stage and appropriate clinical action plan.
- Most labs will provide the GFR, we won't be asked to calculate the values on a test. ******GFR is the best overall index of kidney function
White blood cell casts: Formed when WBC's incorporated within protein matrix - enter the urine stream by ameboid movement through and between tubular epithelial cells and sometimes across the glomerular capillary lumen; associated with diseases with leukocytic exudation and interstitial inflammation (e.g., pyelonephritis.

- Red cell casts: Formed from RBC's packed in fibrin meshwork within cast matrix occurring as a result from severe injury to the glomerular basement membrane; associated with acute glomerulonephritis (most common), lupus nephritis, Goodpasture's syndrome, and subacute bacterial endocarditis.
Renal epithelial casts: Result from constant desquamation and renewal of the renal epithelium - pathological process resulting in damage to the tubular portion of the nephron (tubular damage); associated with nephrotoxic agents and exposure to some viruses.

- Granular casts: Formed from breakdown products of cellular casts and immunoglobulins - include coarsely granular and finely granular casts. Deeply pigmented (i.e., muddy brown) granular cast are characteristic for acute tubular necrosis!

Waxy casts: Result of progressive degenerative changes in cellular casts; associated with severe chronic renal disease and amyloidosis.

Fatty casts: Commonly attributed to leakage of lipoproteins through glomerular filter; associated with nephrotic syndrome, diabetes mellitus, and damaged renal tubular epithelial cells.
- *know what deeply pigmented/muddy brown granular casts are characteristic of!!!!!!!!!!!!!= ACUTE TUBULAR NECROSIS!!!

Oval Fat Bodies and Fatty Casts:
- Transitional Epithelial Cells

B: Oval Fat Body (note lipid drops within body)
- Oval Fat Bodies and Fatty Casts: Renal tubular cell or cast containing fat globules suggestive of nephrotic syndrome. Under polarized light fat bodies reveal "maltese cross" appearance. Lipid deposits can appear as isolated fat deposits, oval fat bodies, and fatty casts, and can be seen together on same urine sample.
- Oval fat bodies hovering around the urine sample along with the fatty cast and fat droplets as well, often see all 3. the fat in the cells tells us elevated lipids
Glomerular Filtration Rate (GFR) :
- Rate of glomerular filtration (i.e., GFR) is major determinant in creatinine excretion and, therefore, renal function. The lower the GFR, the lower the creatinine excretion, and the higher the plasma creatinine.

Therefore, and generally speaking, there is an inverse relationship between GFR and plasma creatinine values such that:

↓GFR=↑Creatinine Level
↑GFR=↓Creatinine Level
-However, given variance in muscle mass and food intake (both affect creatinine) and normal variances in creatinine level the relationship between reduced GFR and creatinine level is not linear.
1 : Rise in serum creatinine from 1-2 mg/dl = 50% reduction in GFR
2 : Rise in serum creatinine from 4.7-6mg/dl = ≈5% reduction in GFR
- A similar relationship exists between BUN and GFR
-As urea is primarily excreted via glomerular filtration, changes in the GFR can change plasma urea levels.
-However, this, too, is not linear - the GFR must be significantly reduced to result in an increase BUN as urea excretion not determined solely by glomerular filtration (Up to 50% of filtered urea is normally reabsorbed from the tubules, passively following water and sodium).
-BUN alone is not a reliable indicator of changes in the GFR
-Urea production not always constant (formed by hepatic metabolism of amino acids - BUN increases with increased hepatic metabolism of amino acids) Can occur with dietary changes (e.g., increased protein intake), greater tissue breakdown (e.g., trauma), and medication use leading to decreased protein synthesis (e.g., tetracyclines).
KIDNEY DISEASE: Laboratory Evaluation
Diagnostic Test Results Associated Causes
Elevated Creatine Kinase and Myoglobin Rhabdomyolysis
Elevated Uric Acid Gouty Neprhopathy, Malignancy
Elevated Calcium Malignancy
Monocolonal Spike on Serum Protein Electrophoresis Multiple Myeloma
Hemoglobin SS on Hgb electrophoresis Sickle Cell nephropathy
Positive HIV Testing HIV Nephropathy
Elevated Antistreptolysin-O titer Poststreptococcal Glomerulonephritis
Evidence of Hemolysis (schistocytes on peripheral blood smear, decreased haptoglobin, elevated indirect bilirubin, elevated lactate dehydrogenase, thrombocytopenia) Hemolytic Uremic Syndrome, Thrombocytic Thrombocytopenic Purpura, SLE, other autoimmune diseases
Positive ANA Autoimmune Diseases
- - Do Ck b/c-...
ASO- make sure that its not from strep, also check psych pts with OCD
- Diagnostic Test Results Associated Causes
Low complement level SLE, endocarditis, postinfectious glomerulonephritis
Positive antibasement membrane antibody Good pasture's Syndrome
Positive cytoplasmic antineutrophil cytoplasmic antibody Wegener's Granulomatosis
Increased anion gap with increased osmolar gap Ethylene Glycol or Methanol Poisoning
Eosinophilia Allergic Interstitial Nephritis
Positive blood cultures and new cardiac murmur Endocarditis
Elevated Prostate-Specific Antigen Prostatic Hypertrophy, Prostate Cancer
Abdominal Calcifications on Plain-Film Radiograph Nephrolithisis, Ureterolithiasis
Mass or Calcifications on Abdominal or Pelvic CT and Hydronephrosis on Ultrasound Malignancy, Prostatic Hypertrophy, Uterine Fibroids, Nephrolithiasis, Ureterolithiasis
1. Elevated Uric Acid- Gouty Neprhopathy, Malignancy
2. Creatine Kinase and Myoglobin-Rhabdomyolosis
3. Elevated Calcium-Malignancy
4. Monocolonal Spike on Serum Protein Electrophoresis
-Multiple Myeloma
5. Hemoglobin SS on Hgb electrophoresis- Sickle Cell nephropathy
6. Positive HIV Testing- HIV Nephropathy
7. Elevated Antistreptolysin ~ O titer-Poststreptococcal Glomerulonephritis
8. Evidence of Hemolysis (schistocytes on peripheral blood smear, decreased haptoglobin, elevated indirect bilirubin, elevated lactate dehydrogenase, thrombocytopenia)- Hemolytic Uremic Syndrome, Thrombocytic Thrombocytopenic Purpura, SLE, other autoimmune diseases
9. Positive ANA- Autoimmune Diseases

(note---Do Ck b/c-...
ASO- make sure that its not from strep, also check psych pts with OCD)
10. Low complement level-SLE, endocarditis, postinfectious glomerulonephritis
11.Positive antibasement membrane antibody-Good pasture's Syndrome
12.Positive cytoplasmic antineutrophil cytoplasmic antibody-Wegener's Granulomatosis
13.Increased anion gap with increased osmolar gap-Ethylene Glycol or Methanol Poisoning
14.Eosinophilia- Allergic Interstitial Nephritis
15.Positive blood cultures and new cardiac murmur-Endocarditis
16.Elevated ProstateSpecific Antigen (PSA)- Prostatic Hypertrophy, Prostate Cancer
17.Abdominal Calcifications on Plain-Film Radiograph-Nephrolithisis, Ureterolithiasis
18.Mass or Calcifications on Abdominal or Pelvic CT and Hydronephrosis on Ultrasound-Malignancy, Prostatic Hypertrophy, Uterine Fibroids, Nephrolithiasis, Ureterolithiasis
Stage #-Description-GFR range (mL/min/1.73m2)

Stage 0: At Increased Risk= ≥90.
Stage 1: Kidney Damage with normal or increased GFR
=≥90.
Stage 2: Kidney Damage with mildly reduced GFR(GFR starts dropping) = 60-89.
Stage 3: Moderately reduced GFR = 30-59
Stage 4: Severely reduced GFR (plan for dialysis)
= 15-29
Stage 5: Overt renal failure -start dialysis = <15

-Stage 0 great predictor for later disease, stage 0-indicates need to be aggressive, doing fine but at risk for developing renal disease later on. Keeps you alert and monitoring the pt. can help prevent the development of the disease. LDL below 100 for cardiac
-Adapted from National Kidney Foundation Kidney Disease Outcomes Quality Initiative Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification. http://www.kidney.org/professionals/kdoqi/guidelines_ckd/p9_approach.htm
- On dialysis makes your GFR appear to go up.

Stage 1: kidney damange and normal or increased GFR
Stage 2: Kidney damage and mild decreased GFR
Stage 3: moderate decrease in GFR
Stage 4: Severe decrease in GFR
Stage 5: KIDNEY FAILURE - dialysis!

STAGE ACTION PLAN/ CKD Clinical action plan:
Stage 1= DX & TX, Tx of comorbid conditions, Slowing the progression, Cardiovascular risk reduction.
- Stage 2 Estimating progression
Stage 3- Evaluate & TX complications
Stage 4 - preparation of kidney replacement therapy ( pt and family education, dialyisis access, preemptive transplant
Preemptive transplant is stage 4 prophylactic alive kidney!!!
- Stage 5- Kidney replacement therapy (if clinically indicated)
MARY: 70yo black female
MHX: HTN ( 141/85), osteoarthritis, DM2 & hyperlipidemia. Experiencing fatigue, evening cramping, and difficulty urinating, worsening GFR recently noted!
SHX: nursing home resident, non-smoker, experiences decreased mobility from arthritis, daughter lives out of state
RX's: Lisinopril (decreases sugars) 5 mg po BID
Hydrochlorothiazide 25 mg qd
Clonidine 0.1 mg po BID
Glipizide 5mg qd
Simvastatin 20mg qd
Ibuprofen
- ddx- acute renal failure, worsening chronic condition, renal calcilie, CV disease, *70 yr should not be on an NSAID.
-LABS:
HbA1c- 7.9%
Pre-Prandial glucose- 141
Peak post-prandial glucose - 191
Total cholesterol - 214
LDL- C 164
HDL-C 51
Triglycerides 171
HG - 11.5
Bicarb- 25 mmol/L
BUN 35
Spot Urine Protein/ Creatinine ration = 320 mg/g
Creatinine - 1.3
eGFR - 51
-Increased BUN and Creatinine, what stage is this pt in? !!!!!!!!! A normal serum creatinine does not rule out kidney disease, a very hammered pt. !!!!!!!
Spot urine and protein are tests of chronic kidney disease, wouldn't test these for acute.
-WHAT ARE MARY"S CKD RISK FACTORS?
A) Older Age
B) HTN
C) Use of NSAIDS
D) All of the Above ****************!!! D= correct

-What would indicate that Mary has clinical proteinuria?
A)<20mg/dL spot urine dipstick
B) >300mg/d total protein (24hr excretion)
C)<200 mg/g spot urine protein-creatinine ratio
D) None of the above
=== Correct = B !!***** >300 mg/d total protein (24 hr excretion) would indicate that Mary has clinical proteinuria
Difference btw spot and 24hr collection and the albumin to cr ratio!

-An e GFR of 51 ml/min/1.73m would indicate that mary has ____?
A) Stage 1
B) stage 2
C) Stage 3******* c=correct1
D) Stage 4
Malnutricion and CKD:
Malnutricion or protein energy wasting (PEW) is common on CKD associated w/ poor pt outcomes!
Malnut in CKD begins as early as stage 3 and 4 !!!!!!. Risk increases w/disease progression.
- preventing PEW or malnutricion may require clinical intervention to assess nutricional status, individualize strategies for prevention and tx and to provide pt instruction and to promotes pt adherence
- special trained registered dietician can help address the nutricional aspects so that protein wasting can be avoided or diminished
-People with CKD often have high phosphorus and high K, often start diaylsis when you can no longer control these levels and keep them down, you try to keep people w/ CKD at lower levels K normal is 4 but people w/ CKD keep them around 2 when they're in stages 3-4. rxs given to leach these out of your blood. If phos is high then your ca is usually lower... Phosphorus and K and GFR and the 3 main thing that determine when you have to start someone one dialysis. Gfr >15, elevated K >4 if stages 1-2 or 3-4 >2.4. phos is : ( for kidneys. Dairy phos and Ca watch out.

- -A balanced approach to nutrition in CKD: Macronutrient Composition and Mineral content stages 1-4
Nutrient :
Na - stage 1-4= <2-3
Total fat (% of calories) stage 1-4 = <30
Saturated fat stage 1-4 = <10
Cholesterol stage 1-4 = <200
Carbohydrates stage 1-4 50-60

Protein (g/kg/d, % of calories):
-No diabetes stage 1-2 = 1.4 (~18) ; Stage 3-4 = 0.6-0.8 (~8*10)
-Diabetes stage 1-2 = 0.8 (~10) ; stages 3-4 = 0.6-0.8 (~8*10)

Phosphorus (g/d) stage 1-2 = 1.7 ; stages 3-4 = 0.8-1.0

Potassium (g/d) stages 1-2 = >4 ; stages 3-4 = 2.4

DASH diet = dietary approach to stop HTN diet.
-adjust total calories from protein, fat, carbs, are 100%. Emphasize whole food sources= veggies, whole grains, nuts, legumes, low fat or non fat dairy canola oil olive oil cold water fish and poultry
Normal Renal Ultrasound Findings:
Length: 100-115mm
Width: 50-70 mm
Depth: 30-50 mm
-Renal Parenchyma (i.e., functional tissue of the kidneys) , Measured from the convex outer edge to the tip of a papilla, Normal value = 13-18 mm.
- Kidney Volume calculation (length x width x depth x 0.5). Normal volume = 110-200
- Renal Parenchyma Pyelon Index
(relationship between dorsal parenchyma to pyelon to ventral parenchyma). Normally 1:1:1
Increasing age, renal atrophy results in an index of 1:2:1
- Anatomy
Bean shaped organ with smooth convex lateral organ boundary. Homogeneously hypoechoic renal parenchyma. Hyperechoic surrounding fat tissue and pyeloliceal system with parapelvic fat
- Kidneys have significant anatomical variations - can lead to confusion in US imaging
Tumor-like lesions need F/U with CT
-Polycystic kidney disease, usually large kidney. Small size usually/suggestive of CKD, cells die and kidney shrinks (can be large too). Poly cystic kidney cysts can be ill defined and indeterminable from masses, malignancy, stones, want to see the density. Want to order a helical CT to evaluate.

Normal Sonographic Appearance:
- Bean shaped organ with smooth convex lateral organ boundary
Depending on imaged axis, sonographic shape differs
Longitundinal: Football-shaped
Transverse View: C-shaped
Bright area surrounding kidney: Gerota's fascia and perinephric fat
Grainy gray periphery: Renal cortex and pyramids (pyramids not always identifiable
Echogenic (bright) central area: Renal sinus (calyces, pelvis, renal sinus fat)
Tubular structure extending inferiorly: Ureters (visualized when distended; not always visible when not distended)
-Always scan both kidneys for comparison and correlation to clinical presentation
-Kidneys have significant anatomical variations - can lead to confusion in imaging
-Tumor-like lesions need F/U with CT

Scan both kidneys to compare symmetry and size, congenital abnormalities, assess hydronephrosis (both, rarer but better prognosis)
;