Mohit Rana

VHK-1233
Vth BVSc. & AH.

Chronic renal failure (CRF)

Occurs when compensatory mechanisms

of the diseased kidneys are no longer

able to maintain the EXCRETORY,
REGULATORY, and ENDOCRINE functions
of the kidneys
Resultant retention of nitrogenous
solutes, derangements of fluid, electrolyte
and acid-base balance, and failure of
hormone production constitute CRF

Causes of CRF in dogs

Chronic tubulointerstitial nephritis of unknown cause
Chronic pyelonephritis
Chronic glomerulonephritis
Amyloidosis
Familial renal diseases
Hypercalcemic nephropathy
Chronic obstruction (hydronephrosis)
Sequel to acute renal disease (e.g., leptospirosis)

Differentiation of CRF from

ARF
Renal size
History of previous PU/PD
Non-regenerative anemia
Weight loss and poor haircoat
Parathyroid gland size on
ultrasound
Hyperkalemia

Factors contributing to the

progressive nature of renal
disease
Species differences and extent of reduction

in renal mass
Functional and morphologic changes in
remnant kidney
Time followed
Dietary factors
Systemic complications of renal insufficiency
Therapeutic interventions

Progression of renal disease:

Functional and morphologic changes
in remnant renal tissue
Hyperfiltration increases movement of

proteins across glomerular capillaries

into Bowmans space
Increased protein is toxic to the kidney
End result may be glomerular sclerosis
and tubulointerstitial nephritis

Diet and progression of renal

disease: Protein restriction
Role of low protein diet in slowing

progression of renal disease is

controversial
Prevention of hyperfiltration by low
protein diet may not be feasible in dogs
without inducing malnutrition
Low protein diets may have other
beneficial effects (limitation of
proteinuria)

Diet and progression of renal

disease: Phosphorus restriction
Slows progression of renal

disease
Prevents or reverses renal
secondary hyperparathyroidism
Limits renal interstitial
mineralization, inflammation
and fibrosis

Diet and progression of renal

disease: Lipids
6 PUFA may hasten progression of

renal disease whereas 3 PUFA are

renoprotective
3 PUFA promote production of
good prostaglandins and limit
production of bad prostaglandins

Beneficial effects of 3 PUFA in

renal disease
Decreased cholesterol and

triglycerides
Decreased urinary eicosinoid
excretion
Decreased proteinuria
Preservation of GFR
Less severe renal morphologic
changes

Progression of renal disease:

Systemic complications of renal
insufficiency
Systemic hypertension
Urinary tract infection
Fluid, electrolyte, and acid-base

abnormalities

BUN, creatinine
Azotemia does

not develop
until 75% or
more of the
nephron
population has
become nonfunctional

Anemia of CRF
Non-regenerative (normochromic,

normocytic)
Variable in magnitude and
correlated with severity of CRF (as
estimated by serum creatinine)
Serum EPO concentrations are low
to normal

Gastrointestinal disturbances in
CRF
Oral lesions
Foul odor
Stomatitis
Erosions and

ulcers
Tongue tip
necrosis (fibrinoid
necrosis and
focal ischemia)

Gastrointestinal disturbances in
CRF
Gastric lesions

Back diffusion of acid

Bleeding due to

platelet dysfunction
Bacterial NH4+
production from urea
Ischemia due to
vascular lesions
Increased gastrin

Clinical history in CRF

Findings are non-specific
Polyuria and polydipsia
Vomiting
Anorexia
Weight loss
Lethargy

Physical findings in CRF

Weight loss
Poor haircoat
Oral lesions (most common in dogs)
Pallor of mucous membranes
Dehydration
Osteodystrophy (young growing dog
with familial renal disease)
Ascites or edema (consider
glomerular disease)

Laboratory findings in CRF

Nonregenerative anemia, lymphopenia
Azotemia (75% loss of nephrons)
Hyperphosphatemia (85% loss of

nephrons)
Decreased serum HCO3-

Progression of renal disease:

Therapeutic interventions
ACE inhibitors (e.g. enalapril)
Decrease proteinuria
Decrease blood pressure
Limit glomerular sclerosis
Slow progression
Low protein diet
Decrease proteinuria
Limit urea production
May not limit hyperfiltration

Conservative medical management of

CRF

Free access to water at all times

Protein and calories
Sodium chloride
Alkali and potassium and replacement
Phosphorus restriction
H2 receptor blockers
Hormone replacement (erythropoietin, calcitriol)
Anabolic steroids
Blood pressure control
Avoid stress (SQ fluids at home by the owner)

Medical Management of CRF:

H2 Receptor Blockers
Decrease gastric

acid secretion
Cimetidine

(5 mg/kg q12h)
Ranitidine
(2 mg/kg q12h)
Famotidine
(1 mg/kg q24h)

Medical Management of CRF:

H2 Receptor Blockers

Famotidine
Once per day

dosing
1 mg/kg

Medical Management of CRF

Hormonal Replacement: Erythropoietin
Effects in treated

dogs and cats

Resolution of anemia
Weight gain
Improved appetite
Improved haircoat
Increased alertness
Increased activity

Medical Management of CRF

Hormonal Replacement: Calcitriol
Enhances

gastrointestinal
absorption of calcium
and corrects ionized
hypocalcemia
Reduces PTH
secretion by
occupying calcitriol
receptors on
parathyroid glands

Medical Management of CRF:

Treatment of Hypertension
Amlodipine
0.18 mg/kg in dogs

or 0.625 to 1.25 mg
per cat PO q24h
Recheck BP one
week after starting
drug

Medical Management of CRF:

Treatment of Hypertension
Enalapril
0.5 mg/kg q12h or

q24h
Effect on blood
pressure may be
modest
May have other
potentially
beneficial effects
on kidney