Dr Ajay Katoch

Assistant Professor, Veterinary Medicine

Introduction

The kidneys are

responsible for the

excretion of nitrogenous

and other metabolic

waste products and for

the regulation of water,

electrolyte and acid-base

balance

The kidney has a biosynthetic role,

and is involved in the production of

renin, erythropoietin, prostaglandins

and Vitamin D3

Gluconeogenesis under conditions

of starvation and is an important site

for degradation of some peptide

hormones

Essential terminology

Renal disease

Renal failure

Azotemia

Uremia

Renal disease

Implies the presence of histological lesions in the kidney but does not specify any degree of renal dysfunction

Renal failure

Inability of the kidney to maintain the homeostasis leading to :

The buildup of the nitrogenous waste in blood (azotemia)

The loss of urine concentrating ability

Disturbances of fluid, electrolyte, and acid-base balance

75% of the total nephron population has become non-functional

Azotemia

Increased concentration of non-

protein nitrogenous waste

products (e.g. urea, creatinine) in

the blood

Uremia

Uremia is the poly systemic toxic

syndrome, which develops with

the progression of renal failure

and is characterized by the

presence of clinical signs in

association with azotemia

Toxic Substances accumulating in uremia

Sr. No. ACCUMULATING

SUBSTANCE

ADVERSE EFFECTS

1. Urea Weakness, anorexia, vomiting,

glucose intolerance, bleeding

disorder

2. Guanidine compounds:

1. Guanidine

2. Dimethyl guanidine

3. Creatinine

4. Cretine

5. Guanidinoacetic acid

Weight loss, platelet function defect

6.Guanidinosuccinic acid Interfere with platelet factor III

3. Aliphatic amines:

Dimethylamine

Trimethylamine

Uraemic breath odour,

encephalopathy

Sr.No Accumulating

substance

Adverse effects

4. Polyamine :

i. Spermine

ii. Spermidine

Spermidine reduces erythropoiesis

5. Peptides and polypeptide

hormones

Accumulate due to reduced excretion or

increased secretion occurs as

compensating response to renal failure

6. Parathyroid hormone Osteodystrophy, nephrotoxicity, impaired

erythropoiesis, cardiotoxicity

7. Insulin Hyperinsulinism may lead to islet

exhaustion and diabetes mellitus

8. Glucagon Insulin resistance/ glucose intolerance

Sr. No. Accumulating

substance

Adverse effects

9. Growth hormone Insulin resistance/ glucose intolrence

10. Gastrin Hypergastrinaemia contribute to

gastritis

11. Myoinositol Neuropathy

12. Ribonuclease Impaired erythropoeisis, decreased

cellular proliferation

13. Cyclic adenosine

monophosphate (cAMP)

Abnormal platelet function

14. Derivative of aromatic

amino acids:

i. Trptophan

ii. Tyrosine

iii. phenylalanine

Anorexia

Renal failure

Acute

renal

failure

Chronic

renal

failure

Acute renal failure

Acute renal failure (ARF) describes a sudden reduction in renal function associated with a

sudden decrease in the glomerular filtration rate (GFR) and the rapid development of

azotemia and uremia

Causes

Pre renal (functional )

Shock

Dehydration

Heart failure

Hypoadrenocorticism

Thrombosis of the renal artery or massive blood

loss

Renal intrinsic ( structural)

Acute tubular necrosis

Ischemia Toxin Tubular

factors

Renal intrinsic ( structural)

Acute interstitial Necrosis

Inflammation Oedema

Renal intrinsic ( structural)

Glomerulonephritis

Damage to

intrinsic

mechanisms

Post renal (obstructive)

Urolithiasis

Neoplasm

Herniation

Damage to lower urinary tract

Anatomical abnormalities

Some Nephrotoxins causing renal damage

Ethylene glycol (in antifreeze)

Antibiotics: Amino glycosides, Tetracycline,

Cyclosporin

Chemotherapeutics: Amphotericin B, cis-

platinum, Doxorubicin

Heavy metals: Lead, Thallium, Zinc, Arsenic,

Mercury

Hypercalcemia: Malignancies,

Hyperparathyroid, Vitamin D toxicity

Other causes: Carbon tetrachloride,

Chloroform, Iodinated contrast media

Clinical signs of ARF

Hyperkalemia

Nausea/Vomition

Pulmonary edema

Clinical signs of ARF

Ascites

Dehydration

Clinical signs of ARF

Encephalopathy

Kidney pain

Oliguria

Shock

Disseminated intravascular coagulation (DIC)

Respiratory distress

Neurologic disturbances

Coma and death

Other signs include -

Diagnosis

History and clinical signs

Laboratory findings -

i. Rising creatinine and urea

ii. Rising potassium

iii. Acidosis

iv. Hyponatraemia

v. Hypocalcemia

Management of ARF

Early recognition of disease

Identification and treatment of specific underlying cause

Sodium bicarbonate to correct metabolic acidosis

Provide nutritional support – Non protein calories but high quality protein in limited amount

Management of ARF -

Promote urine output if still anuric.-

Frusemide, Mannitol

Dialysis to remove excess fluid &

waste products.

Gastric protectants and anti-emetics to

alleviate gastrointestinal disturbances

Emergency management of Hyperkalemia

TREATMENT MECHANISM & SPEED

OF ACTION

POSSIBLE ADVERSE

EFFECTS

10% calcium

gluconate

(0.5-1ml/kg)

Protect myocardium

Immediate and short lived

effect

Administer IV slowly ,

overdose can lead to

rhythm disturbances

Sodium

bicarbonate

(1-2 mmol/kg)

Correct metabolic acidosis

so lower plasma K+

15-30 min to work

Overcorrection can lead to

hypocalcaemia, tissue

hypoxia, paradoxical CSF

acidosis

Glucose

insulin

(2gm of

glucose

1 unit of

soluble insulin

per kg)

Glucose stimulate

endogenous insulin

release, insulin stimulate

uptake of glucose and K+

15-30 min to work

Insulin may be dangerous

in case of Addison’s

disease

Chronic renal failure

Chronic renal failure is a relatively common

syndrome in older dogs and represents the end

stage of a number of renal disease

Clinical signs of CRF are not usually apparent

until at least 65% to 75% of renal tissue is

destroyed; so early cases often go undetected

Cause

Pyelonephritis

Chronic nephritis

Renal amyloidosis

Renal urolithiasisHydronephrosisPrimary renal

neoplasia

Glomerulonephritis

Clinical signs

Polyuria and Polydipsia

Weight loss/loss of

muscle mass/poor hair coat

Anorexia with vomition

Weakness, lethargy & depression

Pallor & dryness of mucous membranes

Oral ulceration

Clinical signs

Hypertension

Diarrhoea

Pruritis (itching)

Edema

Anaemia

Neurologic changes

Diagnosis

I. History

II. Clinical findings

III. Laboratory findings:

Urinalysis-

Sp. gravity<1.025

Proteinuria, WBC,RBC

Blood- Lymphopenia, Non-

regenerative anaemia.

Red blood cast

WBC cast

Diagnosis :IV. Blood Biochemistry:

Blood urea >40mg/dl

Creatinine level > 2mg/dl

Elevated phosphorus level

Elevated Cholesterol

Elevated or decreased calcium level

Acidosis

Diagnosis

Radiography

Bilateral reduction in size of kidney & radio

opaque uroliths

Diagnosis

Ultrasound

UrolithiasisPolycystic renal

disease Hydronephrosis

Management of CRF

Fluid therapy

Dietary restrictions

(protein; phosphorus) -

Protein intake should be

low but first class protein

should be provided to

prevent tissue breakdown.

Calcium supplements

Management of CRF

Blood pressure treatment: Angiotensinconverting enzyme (ace) inhibitors - e.g. enalapril / vasotec

Gastrointestinal protectant

Dialysis

Kidney transplant

Drug to be avoided in RF

Aminoglycosides

Nalidixic acid

Aspirin

Amphotericin

Neomycin

Nitrofurantoin,

Sulphonamides

Tetracycline and Magnesium salt

Acute Vs Chronic failure S.no Parameter Acute Chronic

1. History Perfectly healthy

until very recently

Weeks to months of

polyuria / polydipsia,

weight loss & vomition

2 Physical

examination

Good body

condition.

Extremely

depressed relative

to the degree of

azotaemia

May be cachectic.

Tolerates severe

azotaemia rather well

3 Kidney size Normal sized or

large – may be

painful

Small & non painful.

Chronic disease like renal

neoplasia, polycystic

kidneys, hydronephrosis

S. no Parameter Acute Chronic

a) PCV Anemia is not usually

present

Non-regenerative

anemia

b) Potassium,

Phosphate and

Acid/base

Hyperkalaemia,

hyperphosphataemia

and metabolic

acidosis

No Hyperkalaemia,

Hypokalaemia may

occur

c) Urinalysis Sediment contains

casts, cells, debris

etc.

Urine sediment is

inactive.

d) Urine production Anuric or oliguric

mainly

Polyuric

e) Response to

therapy

Often reversible Irreversible

Breeds prone to Renal Failure

Bull terrier

Doberman Pinscher

Breeds prone to RF

Lhasa Apso Norwegian Elkhound

Soft coated wheaten terrier

Breeds prone to RF

Standard poodle Cairn terrier

Beagle