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OS 214 CHRONIC RENAL FAILURE 1/3

EXCRETORY dR. IRMINGARDA GUECO, MARCH 6, 2005
GROUP

OUTLINE 5 Renal Failure (ESRD) < 15

1. Discuss the pathophysiology of CRF/ESRD.
2. Distinguish the pathophysiology of CRF from ESRD.
3. Describe the clinical manifestations of CRF/ESRD.
4. Correlate clinical history and physical examination GFR
findings with the pathophysiology of CRF/ESRD. • CRF: 16-89 mL/min
5. Discuss the laboratory findings in CRF/ESRD.
• ESRD: <15 mL/min
6. Discuss the supportive management of patients with
CRF/ESRD.
7. Explain the principles and indications of renal Difference between CRF & ESRD in terms of
replacement therapies, including renal transplantation. Pathophysiology
8. Construct an algorithm on the approach to a patient with
CRF/ESRD.
We would like to acknowledge the KREMLINS for the soft
CRF – there is hyperfiltration, some amount of
copy of this trans  Notes taken during the lecture are in arial compensation
size 8
ESRD – no more compensation; all other organ
Why separate acute from chronic renal failure? systems will end up with some kind of dysfunction
- Management is different
- Manifestations may be similar Kidney Chronic Renal End-Stage Renal
- Prognosis is different: Chronic Renal Failure Function Failure (CRF) Disease (ESRD)
– irreversible; Acute Renal Failure – reversible Excretory No signs / Nausea /
Function symptoms vomiting
Functions of the Kidney Measured ↑ BUN ↑↑ BUN
using: ↑ Creatinine, ↑↑ Creatinine,
Excretory function BUN, ↑ Cystatin C ↑↑ Cystatin C
creatinine
pH, HCO3,
Maintenance No ↑ RR – Kussmaul
Maintenance of Acid – Base Balance
pCO2 of Acid- Manifestations breathing
Maintenance of Fluid and Electrolyte Osmolality, Base Normal acid- Metabolic
Balance water, Na, K, Balance base balance Acidosis
Cl
Maintenance ↑ RR
Maintenance of Ca-Phosphate Balance Ca,
Phosphates of Fluid & ↑ BP Arrythmia
(Mineral balance) (Mg) Electrolyte NVE NVE
Vitamin D production Calcium Balance Crackles Crackles
Erythropoeitin Production Hgb, hct for Edema Edema
confirmation Na – Normal Na – Normal
K – Normal or ↑ K–↑
Chronic Renal Failure (CRF) Maintenance No Osteitis fibrosa
of Calcium- manifestations cystica
-Pathophysiologic process which is a result of varied Phosphate ↑ Phosphate ↑↑ Phosphate
conditions that leads to irreversible destruction of Balance ↓ Ca ↓↓ Ca
nephrons, ultimately leading to End Stage Kidney Vitamin D No Osteomalacia
Disease (ESRD). Production manifestations ↓ Calcitriol
-Sum of all processes that happen cause by various diseases such ↓ Calcitriol
as DM, hpn, GN, lupus, secondary causes due to multiple myeloma,
etc.
(see diagram
- Slow deterioration of kidney function below)
- Loss of nephrons  other nephrons try to compensate Erythropoietin Weakness Weakness
during CRF phase, you don’t see manifestations of ESRD Production Dizziness Dizziness
- Normal GFR men:100ml/min; women:85ml/min
- Just keep in mind that the key word in CRF is COMPENSATION
Pallor Pallor
- DO NOT MAKE THE MISTAKE OF DIALYSING A PATIENT WITH Easy Fatigability Easy Fatigability
CRF! ↓ Hemoglobin ↓↓ Hemoglobin
Spectrum of CRF: Excretory function:
• ≤1.5mg creatinine
Normal kidney CRF (>3mos) ESRD • 10-20 BUN depending on level of hydration
• Cystatin- only used in lab research for now
Pathophysiology Maintenance of Acid-Base Balance:
-Long term reduction of renal mass / function which • Still with compensation
initially leads to compensatory hypertrophy and Maintenance of Fluid & Electrolyte Balance:
function. Eventually this leads to sclerosis of the • For fluids, think also of sodium going along with it
remaining nephron, resulting to ESRD. • Creatinine clearance >60, accumulation of Na
• Increased BP: CM, lupus, GN
Stages of Chronic Renal Disease • No signs/symptoms, normal BP: may also have renal failure,
creatinine worsening
Stage Description GFR, mL/min per • Buko juice: causes hyperkalemia; so AVOID DRINKING BUKO
1.73 m2 JUICE WHEN YOU HAVE KIDNEY PROBLEMS UNLESS YOU
1 At increased risk of 90 (with CRD risk HAVE LOW POTASSIUM
kidney damage with factors) • Buko juice, bananas  good fore people with diarrhea
normal or increased GFR 90 • Nephrologists should therefore identify patients are Na or K
wasters. If this is the case then don’t let them avoid Na of K.
2 Kidney damage with 60-89 Maintenance of Calcium-Phosphate Balance
mildly decreased GFR • >25% creatinine clearance is still normal
3 Moderately decreased 30-59 Vitamin D Production
GFR • Calcitriol- only in lab research for now
4 Severely decreased GFR 15-29 • (Please refer to table at last page) Why is there an increase in
phosphates in ESRD?  because the poorly functioning kidney
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OS 214 CHRONIC RENAL FAILURE 2/3
EXCRETORY dR. IRMINGARDA GUECO, MARCH 6, 2005
GROUP

can’t eliminate them all. The phosphate binds with calcium  Pathophysiology: fibrosis – no more compensation in
leading to a decrease in ionized calcium  leading to whatever aspect of excretion
secondary hypoparathyroidism
Erythropoietin Production
• In DM, anemia occurs early Management of ESRD
A. Supportive
Management of Chronic Renal Failure 1. Nutrition
2. Psychological
A. Comprehensive strategy for renoprotection in 3. Control BP
patients with chronic renal disease 4. Maintain Hb at 110-120 g/dl with
Intervention Therapeutic Goal erythropoietin oral iron is not absorbed very\well
by uremic patient; it’s better to give it to them IV
Specific renoprotective
therapy Proteinuria <0.5 g/day 5. Fluid and electrolyte balance
ACE inhibitor or ARB GFR decline <2 6. Acid-base homesotasis
treatment ml/min/year 7. Maintain Ca and Phosphate balance – give
Calcium carbonate or Calcium acetate with meals.
Adjunctive cardiorenal You eat meat, and meat has phosphate. Para habang
protective therapy nakakapagbigay ka ng calcium, nakakapag prevent
Additional <130/80 mm Hg ka na rin ng absorption ng phosphate. You “shoot two
birds with one stone”
antihypertensive
B. Renal Replacement Therapy
therapy
1. Dialysis
Dietary protein restriction
2. Hemodialysis
Dietary salt restriction 0.6-0.8 g/kg/day
3. Peritoneal Dialysis
Tight glycemic control 3-5 g/day
4. Transplant
in diabetes
5.
Reduce elevated AIC < 6.05 % - Consider dialysis if creatinine clearance is about 20ml/min
calcium-phosporous Normal values - Uremic symptoms present with nausea and vomiting. If the disease
is not ESRD, consider other etiologies for the said symptoms
Lipid lowering therapy LDC-C <100mg/dl - Excess fluid in the body – volume overload – diuretics won’t help
coz kidneys are already sclerosed
Anti-platelet therapy Thrombosis prophylaxis
Consider correction of Hb > 12g/dl Renal Replacement Therapy in CRF
anemia - indicated when metabolic abnormalities can no
Smoking cessation Abstinence longer be controlled with conservative
Weight control Ideal body weight management or when signs and symptoms of
uremia developed
• Level of proteinuria determines the level of dietary protein
restriction in patients
- No absolute value in terms of CR by which you will
• Reduce elevated electolyte Ca and P if <25%, it merits
start your RRT
checking
• The lecturer considers correction of anemia if Hb 11-12g/dl Indications for Dialysis
• Lipid lowering therapy (Statins) - volume overload
- intractable metabolic acidosis
B. Avoid insults to the kidney - hyperkalemia
- uremic state (encephalopathy, pericarditis)
•Volume depletion- diarrhea - azotemia without uremic manifestations
•Nephrotoxins- aminoglycosides, radiocontrast material
CASE
•NSAID- COX2 inhibitors, mefenamic acid, naproxene,
indomethacin
A 24-year old male diagnosed with chronic
C. Preparation for ESRD management glomerulonephritis was admitted for nausea and
vomiting. Maintenance of ACE inhibitors with HCTZ
• Psychological
(Hydrochlorothiazide) was given.
• Renal Replacement Therapy, options
o Dialysis – Vascular Access His last follow-up a week ago showed a Cr 1.8 mg%.
o Transplant – Recipient Donor Work-Up Three days PTA he had copious diarrhea and was
* with a creatinine clearance of 20 or 25, you unable to take anything including medicines. He noted
can start discussing dialysis with the patient decreased urine output. He felt weak and later
developed nausea and vomiting.
End Stage Renal Disease
Please see table on first page PE: BP = 90/60 PR = 110/min RR = 25/min
Excretory function:
Sunken eyeballs, dry skin and mucous membranes
 Nausea and vomiting- SSX of accumulation of BUN, creatinine
Maintenance of Acid-Base Balance: BUN 80mg/dL; Cr 10mg/dL; K 6meq/L; Na 132 meq/L
• metabolic acidosis ABG: pH 7.2; HCO3 11meq/L; CO2 20meq/L
Maintenance of Fluid & Electrolyte Balance: Hgb: 15gm/dl (N14-17)
• body can’t eliminate waste products because it can’t Hematocrit: 45 (hemoconcentrated)
compensate; arrhythmia due to increased K Urinalysis: Sp gr = 1.010, (4+) protein, (–) sugar
Maintenance of Calcium-Phosphate Balance 4-5 RBCs/hpf, 10-15 WBCs/hpf
• Phosphate retained, binds to Ca, absence of Vit D3 decreased
gut absorption of Ca
Vitamin D Production What is your diagnosis?
Erythropoietin Production a. Acute renal failure
b. Chronic renal failure
•Anemia insidious in onset  so you may have SSX in ESRD c. End stage renal failure
d. Acute on chronic renal failure
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OS 214 CHRONIC RENAL FAILURE 3/3
EXCRETORY dR. IRMINGARDA GUECO, MARCH 6, 2005
GROUP

Answer: Acute on Chronic Renal Failure Answer: Dialysis

What finding tells us that the patient has renal If anemic (Hb 10g/dl), what is the mgt?
failure?
a. K Answer: Give erythropoietin. If <10 g/dl, transfusion
b. pH
c. creatinine
From block B:
d. urinalysis –just a reflection that something’s wrong, but
not specific for renal failure  Hyperkalemia – don’t give diuretics because patient is
dehydrated; give sodium bicarbonate -> push K inside
the cell, decrease K levels contraindication of sodium
Answer: Creatinine bicarbonate: presence of NVE, crackles, edema
 Hydration removes hemoconcentration. After hydration,
What is the cause of the ABG finding? observe true level of Hgb. If low Hgb -> address
anemia.
e. Chronic GN
 If Pt does not improve -> Ultrasound, check for other
f. Diarrhea renal problems
g. Vomiting
h. Acute renal failure

Answer: Diarrhea and ARF (acidosis)

How should you manage this patient?

a. kidney transplant
b. dialysis
c. supportive management
d. observe

Answer: Supportive Management

Management:
 Hydrate patient
 For increased K, give sodium bicarbonate- shoot two birds with
one stone  not only do you decrease K you also replace the
lost HCO3
 Treat the cause of diarrhea
 Nutrition: don’t focus on it yet. Just follow treatment for diarrhea
 Follow up BUN, creatinine. If it improves, don’t do anything.
Take note that there’s a 3-4 day period before creatinine drops.

Hypovolemia: low BP, sunken eyeballs, dry skin, mucous membrane

Increased RR implies metabolic acidosis
Hemoconcentration due to diarrhea

If the creatinine changed from 1.8 to 9mg, but the

patient has nausea and vomiting, Bp=130/80, no
diarrhea, eyeballs not sunken, (+)edema, what is
the management?

Decreased Renal Function

Hyperphosphatemia Decreased 1.25 Accumulation of

(OH)2D3 AI3+ Intoxication
ß2 microglobulin

Decreased ionized
Ca2+
Decreased
expression
of calcium-
sensing Hyperparathyroidism
receptor

Hyperplasia
of the
parathyroid
glands

Osteitis fribrosa cystica Osteomalacia Adynamic bone Dialysis-related

(high-turnover bone disease) disease amyloidosis

Metabolic acidosis Excess Ca and vit D, PD, diabetes