Chapter 77 Diseases of the Kidney and Ureter

ACUTE RENAL FAILURE

Acute renal failure (ARF) is a syndrome caused by an abrupt decline in renal function that occurs over a period of hours to days. Clinical signs result from inability of the kidneys to excrete metabolic wastes and adequately regulate fluid, acid, base, and electrolyte balance. Consistent laboratory findings include azotemia with decreased urine concentrating ability (urine specific gravity usually <1.025).

Key Point

When azotemia is identified, it is important to distinguish among prerenal, renal, and postrenal causes.

• Prerenal azotemia can result from any disorder that decreases renal perfusion (e.g., dehydration, heart failure, or hypovolemia) or that results in increased production of urea (e.g., gastrointestinal hemorrhage). With few exceptions (Table 77-1), dogs and cats with purely prerenal causes of azotemia pro-duce concentrated urine (i.e., specific gravity >1.035 in dogs and >1.040 in cats). In addition, prerenal azotemia quickly resolves when the cause of decreased renal perfusion is corrected (e.g., fluid therapy).

• Renal azotemia is caused by renal failure and occurs when 75% of nephrons are nonfunctional. Dogs and cats with renal failure have concomitant azotemia and inability to adequately concentrate urine. Isosthenuria (specific gravity of 1.008–1.012) often exists, and urine specific gravity (USG) is almost always <1.025, although some cats with renal failure maintain ability to concentrate urine up to 1.035. In contrast with prerenal causes, renal azotemia usually does not resolve quickly with treatment.

• Postrenal azotemia results from decreased elimination of urine from the body, most often due to urethral obstruction or a rupture in the urinary system. There usually is something in the history (e.g., trauma or stranguria) or physical examination (e.g., abdominal fluid, swelling or discoloration of the perineal area, or masses within the prostate, urethra, or urinary bladder) that suggests a postrenal cause of azotemia. Additional tests such as radiography (plain and contrast), ultrasonography, and abdominal fluid analysis are helpful in confirming postrenal azotemia. Postrenal azotemia also rapidly resolves after correction of the underlying cause.

Etiology

ARF in dogs or cats results from acute tubular necrosis (i.e., nephrosis) and less frequently from renal inflammation (i.e., nephritis). Acute tubular necrosis is caused by nephrotoxins or renal ischemia (Table 77-2). Nephritis usually is due to infectious diseases in small animals.

• Toxins: Renal tubular toxins are responsible for about 20% to 25% of cases of ARF. Ethylene glycol is responsible for the overwhelming majority of ARF cases due to toxins. Less commonly, drugs (e.g., aminoglycosides) are a cause of ARF.

• Ischemia: Renal ischemia probably causes ARF more often than was once considered. Approximately one-third of dogs with ARF have a condition that predisposes to renal ischemia. In general, renal ischemia is most likely to cause ARF in patients that have preexisting renal disease or that have multiple, concomitant disorders that cause renal injury.

• Nephritis: Nephritis causes ARF in a small number of cases, probably less than 10%. Leptospirosis is the most common infectious cause of ARF (see Chapter 19), but pyelonephritis also may cause ARF, especially if concomitant urinary obstruction exists. Rarely, ARF occurs in dogs with rickettsial infections such as Rocky Mountain spotted fever (see Chapter 17). Recently, Lyme disease has been associated with ARF in dogs (i.e., Lyme nephritis) (see Chapter 18).

• Idiopathic: Even after thorough evaluation, a cause for ARF cannot be identified in approximately 20% to 25% of patients.

Table 77-2 CAUSES OF ACUTE TUBULAR NECROSIS IN DOGS AND CATS

Nephrotoxicosis	Renal Ischemia
*Therapeutic Agents* Aminoglycosides Amphotericin B Tetracycline (IV) Cisplatin Thiacetarsamide Paromomycin Calcitriol analogues Streptozotocin *Endogenous Substances* Hypercalcemia Hemoglobinuria *Other Substances* Ethylene glycol Iodinated contrast agents (IV) New methylene blue (IV) Lily plants Cholecalciferol rodenticide	*Hypovolemia* Dehydration Hemorrhage Hypoadrenocorticism *Decreased Cardiac Output* Congestive heart failure Arrhythmias Anesthesia *Renal Vasoconstriction* ACE inhibitors NSAIDs *Renal Thrombosis* Bacterial endocarditis Disseminated intravascular coagulation

NSAIDs, nonsteroidal anti-inflammatory drugs.

Clinical Signs

Clinical findings in patients with ARF are nonspecific and include lethargy, depression, inappetence, vomiting, and diarrhea. Urine volume varies, and in most cases the patient is presented for other signs before the owner has a chance to observe a change in urinary habits. Most patients with ARF have normal to decreased urine output, although some have polyuria (e.g., aminoglycoside toxicosis).

Diagnosis

Key Point

Make sure to distinguish between ARF and chronic renal failure (CRF) because ARF is a potentially reversible condition that requires aggressive treatment initially.

Distinguish between ARF and CRF on the basis of findings from history, physical examination, and routine laboratory evaluation (Table 77-3). Evaluation of renal size by abdominal radiography or ultrasonography also is helpful. In some cases, a renal biopsy is necessary to make a definitive diagnosis of ARF or CRF.

Table 77-3 DIFFERENTIATION BETWEEN ACUTE AND CHRONIC RENAL FAILURE

	Acute Renal Failure	Chronic Renal Failure
*Clinical Findings*	Acute onset of inappetence, depression, and vomiting (less than 1 week)	Chronic inappetence, vomiting, depression, weight loss (usually weeks to months)
	Usually moderate to severe depression	Often alert, responsive, and only slight depression
	Urine volume often decreased	Polyuria/polydipsia common
	Good body condition	May be thin
	Kidneys enlarged, painful but possibly normal	Kidneys small, irregular but possibly normal
	Bone density always normal	Bone density may be decreased
*Lab Findings*	Normal or increased hematocrit, but anemia may be present	Nonregenerative anemia, but hematocrit may be normal
	BUN and SCr previously normal but increasing progressively	BUN and SCr previously increased and typically stable
	Normal to increased serum potassium	Normal to decreased serum potassium
	Moderate to severe metabolic acidosis	Mild to moderate metabolic acidosis
	Urinary casts in some patients	Urinary casts usually absent
	Proteinuria or glucosuria may result from acute tubular necrosis	Proteinuria often present but usually due to glomerular disease

BUN, blood urea nitrogen; SCr, serum creatinine.

History

• Carefully question owners about potential for exposure to nephrotoxins. Ethylene glycol toxicosis cannot be excluded in any patient that is allowed outdoors, especially in free-roaming pets. Ask the owner if the animal has been given any over-the-counter medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) (ibuprofen, aspirin).

• Ask about the patient’s urine volume. Many dogs and cats with CRF have a history of polyuria/polydipsia (PU/PD), whereas oliguria or anuria usually indicates ARF.

Laboratory Evaluation

Treatment

Key Point

Objectives of treating ARF are to minimize additional renal injury, promote diuresis if oliguria exists, and combat metabolic consequences of uremia.

• With time, renal injury in patients with ARF may be repaired so that there is adequate renal function to maintain homeostasis. This requires 2 to 4 weeks of aggressive medical treatment in many patients.

• Discontinue all potentially nephrotoxic drugs to avoid additional renal injury; if a potentially nephrotoxic drug must be administered, adjust the dosage appropriately. For drugs that undergo renal excretion, dividing the dose by the creatinine concentration or multiplying the dosing frequency (in hours) by the creatinine concentration provides a rough adjustment for the increased exposure to drugs in patients with renal failure.

• Rapidly correct all prerenal factors (dehydration, decreased cardiac output) so that renal perfusion is maintained.

• Administer treatment as necessary to control consequences of uremia such as vomiting, metabolic acidosis, hyperkalemia, and hyperphosphatemia.

• If an underlying cause of ARF or renal injury can be identified (pyelonephritis, leptospirosis), administer specific treatment to eliminate the disorder.

Initial Patient Management

• Determine baseline values for PCV, plasma or total protein, blood urea nitrogen (BUN), serum creatinine, phosphorus, potassium, calcium, sodium, and total carbon dioxide (CO₂).

• Record values for body weight and hydration status. Use body weight after rehydration as a reference for future comparisons.

• Aseptically place an indwelling IV catheter, preferably in a jugular vein. In addition to convenience for the patient, jugular catheters allow collection of blood, measurement of central venous pressure, and IV administration of hypertonic solutions (see Chapter 5).

• If oliguria (i.e., urine volume <1 ml/kg/hr) persists after apparent rehydration, place an indwelling urinary catheter so that urine volume can be objectively measured. Connect the urinary catheter to a closed collecting system. Unless absolutely necessary, avoid administering antimicrobials to patients with indwelling urinary catheters because it may predispose to development of resistant UTI.

Fluid Therapy

A comprehensive discussion of fluid therapy is provided in Chapter 5.

Initial Treatment

• Calculate the dehydration deficit using the following formula to determine volume of fluids (milliliters) to correct dehydration initially:

• If cardiac function is normal, correct dehydration within 6 hours by administering fluids IV.

• Ideally, select the type of fluid on the basis of serum electrolyte concentrations and acid-base status. It usually is safe to use lactated Ringer’s solution in most patients unless hyperkalemia exists. If serum potassium concentration is unknown, initial administration of 0.9% sodium chloride is more appropriate.

• Clinical dehydration may not be apparent in all patients with ARF; however, most of these patients have a history of inappetence, vomiting, and/or diarrhea. Therefore, it generally is safe to assume subclinical dehydration (3–5% of body weight) and treat accordingly. In most cases, it is better to cause slight overhydration than to risk persistent mild dehydration, which may contribute to prerenal azotemia and potentiate ischemic renal injury.

Maintenance Treatment

• After rehydration, the volume of fluids to administer IV for maintenance needs equals the sum of ongoing losses (e.g., vomiting or diarrhea), insensible losses, and urine volume (“in and outs”; see Chapter 5). The fluid rate/volume should be recalculated every 4 to 6 hours to prevent dehydration or hypervolemia.

Key Point

Select a fluid such as Plasma-Lyte M or Normosol-M to facilitate maintenance of normal serum electrolytes. Avoid lactated Ringer’s solution and 0.9% sodium chloride because they contain too much sodium and too little potassium to be maintenance solutions. If a maintenance fluid is not available, alternate lactated Ringer’s solution with 5% dextrose to avoid hypernatremia; add potassium to fluids as needed to maintain serum potassium concentration, especially during the recovery phase of ARF.

• Depending on the severity of renal injury, IV fluid therapy may be necessary for 1 to 3 weeks.

Reversing Oliguria

Key Point

Do not attempt to stimulate diuresis (increased production of urine) with diuretics in patients that are dehydrated or that have non-oliguric renal failure. This will worsen or cause dehydration and electrolyte disturbances, which adversely affect renal function.

If oliguria (<1 ml of urine per kilogram per hour) persists after correction of dehydration, additional treatment is indicated to increase urine production. Urine formation does not necessarily indicate improved renal function; however, it generally is easier to maintain serum electrolytes and acid-base balance in patients that are not oliguric. If there is any doubt whether oliguria exists, place an indwelling urinary catheter so that urine output can be measured.

IV Fluid Therapy

• IV administration of balanced electrolyte solutions promotes diuresis in normal patients and those with non-oliguric renal failure but usually is not effective in patients with ARF.

• Administer fluids to correct dehydration or cause slight volume expansion (3% to 5% of body weight) only and not 1.5 to 3 times maintenance volumes. Patients with ARF cannot adequately handle excessive IV fluids because of acute renal tubular dysfunction and are predisposed to overhydration, which may cause peripheral and pulmonary edema.

Mannitol (20% or 25%)

• Osmotic diuretics such as mannitol are often used initially to stimulate urine production in patients that remain oliguric after rehydration. In addition, mannitol may have beneficial free radical–scavenging properties.

• To avoid thrombophlebitis in peripheral veins it is preferable to administer hypertonic solutions (>10%) through a jugular vein.

• Initially, administer 0.25 to 0.5 g/kg IV over 5 to 10 minutes. If treatment is effective, increased urine production begins within 15 minutes. The goal is to produce 1 to 2 ml of urine per kilogram per hour.

• Continue mannitol every 6 to 8 hours as needed.

• If urine flow does not increase after initial treatment, repeat the dose every 15 minutes up to a total dose of 1.5 g/kg. Do not administer additional mannitol because vascular overload may occur.

Dopamine

• Dopamine often is used to stimulate urine production when patients do not respond to other treatment. Infusion of low doses of dopamine causes dilation of renal vasculature and increased urine production.

• Dilute dopamine in 0.9% saline or 5% dextrose and infuse at a rate of 1 to 3 μg/kg/min using an infusion pump or pediatric infusion set.

• Ideally, a separate IV line should be used so that changes in rate of dopamine infusion can be made without interfering with administration of other IV fluids. However, patients with severe oliguria may need to receive dopamine mixed in a small volume of fluids to avoid overhydration.

• Monitor patients during infusion of dopamine, preferably by continuous electrocardiography, to detect tachycardia or cardiac arrhythmias, which indicate the need to slow the rate of infusion.

• If urine production increases, continue dopamine for 12 to 24 hours or until urine flow can be maintained with IV fluids.

• Continued infusion of dopamine after 6 hours is likely to be ineffective if urine production does not increase.

Dialysis

Hemodialysis is the treatment of choice for ethylene glycol and salicylate toxicosis, life-threatening electrolyte disturbances, severe fluid overload, and cases in which oliguria persists despite measures to stimulate urine production. This requires an intensive care facility equipped for this procedure. For financial reasons, limited availability of hemodialysis, intense labor and complications of peritoneal dialysis, and guarded to grave prognosis for recovery in many cases of ARF, most owners elect euthanasia when dialysis is the only treatment that can maintain their pet.

Managing Electrolyte Disturbances

Hyperkalemia

Hyperkalemia is a potentially life-threatening electrolyte abnormality that occurs in patients with oliguria.

• Serum potassium concentrations between 6 and 8 mEq/L usually do not cause clinically important problems and are best treated by IV administration of 0.9% sodium chloride.

• If serum potassium concentration exceeds 8 mEq/L or if signs of cardiotoxicosis occur (bradycardia, prolonged P-R intervals, absent P waves, tall and peaked T waves, widened QRS complexes, ventricular arrhythmias), other treatment is indicated in addition to IV fluids. Administer sodium bicarbonate (0.5–1.0 mEq/kg) IV over 15 to 20 minutes. Sodium bicarbonate may be preferred in patients with ARF because they often have concomitant acidemia. Sodium bicarbonate causes potassium to move into cells, which lowers serum potassium concentration for several hours.

• Alternatively, administer 0.5 U/kg of regular insulin IV with 1 to 1.5 grams of dextrose for every unit of insulin. This also causes potassium to shift inside cells.

• If life-threatening cardiac arrhythmias exist, administer 10% calcium gluconate (0.5–1.0 ml/kg IV over 10 to 15 minutes) to effect. During treatment, monitor the electrocardiogram (ECG) for shortening of the QT interval and progressive bradycardia, and slow or discontinue calcium infusion if these occur. Calcium gluconate directly antagonizes effects of hyperkalemia on the myocardium for 10 to 15 minutes. It does not affect serum potassium; therefore, concurrent treatment with either bicarbonate or dextrose and insulin is indicated to lower serum potassium.

Hypokalemia

• Hypokalemia may occur during the recovery phase of ARF due to excessive urinary losses and decreased oral intake. Therefore, monitor serum potassium every 1 to 2 days to detect hypokalemia.

• Add potassium chloride to IV fluids as needed to correct hypokalemia (see Chapter 5 for specific guidelines).

Hyperphosphatemia

Hyperphosphatemia occurs secondary to decreased renal elimination of phosphorus in patients with ARF.

• IV administration of fluids helps lower serum phosphorus.

• Additional treatment to control hyperphosphatemia (i.e., feeding a phosphate-restricted diet and administering phosphate binders) can be instituted when the patient tolerates oral feeding.

Correction of Acid-Base Abnormalities

• Metabolic acidosis is the most common and clinically important acid-base disturbance that occurs in patients with ARF. Acidosis occurs because of the kidneys’ inability to reabsorb bicarbonate and excrete hydrogen ions.

• Acidosis predisposes to cardiac arrhythmias, decreased cardiac output, decreased renal perfusion, hyperkalemia, and obtundation.

• Patients with blood pH values above 7.2 or a total CO₂ >12 mEq/L usually respond to IV administration of fluids alone.

• If blood pH is less than 7.2 or the total CO₂ is <12 mEq/L, administer sodium bicarbonate to help normalize acid-base status.

• Calculate the initial bicarbonate dose (mEq) using the following formula: (base deficit) × (body weight in kg) × 0.3. If base deficit is unknown, substitute the value for (20 − total CO₂).

• Administer one-quarter to one-half of the deficit over the first 1 to 2 hours, then add the remaining volume of bicarbonate to calcium-free IV fluids and administer over the next 12 hours.

• Reassess blood gas data or total CO₂ to determine the need for additional bicarbonate therapy. If these values are not available, add bicarbonate at a dosage of 1 to 5 mEq/kg, depending on severity of initial acidemia, to IV calcium-free fluids to be administered over the next 12 to 24 hours.

• Refer to Chapter 5 for a detailed discussion of managing acid-base abnormalities.

Control Vomiting

Vomiting is a common complication of ARF due to effects of uremic toxins on the chemoreceptor trigger zone and emetic center and due to gastrointestinal ulceration, which results from decreased renal elimination of gastrin and subsequent gastric hyperacidity.

• Administer an H₂-receptor antagonist to help control uremic gastritis.

• Administer cimetidine (Tagamet, SmithKline Beecham) IV initially at a dose of 10 mg/kg q12h. As uremia resolves, decrease the dose to 5 mg/kg IV q12h.

• Alternatively, administer ranitidine (Zantac, Roche) at a dose of 2 mg/kg IV q8h in dogs and 2.5 mg/kg IV q12h in cats.

• If vomiting persists, administer a centrally acting antiemetic.

• Metoclopramide (Reglan, Robins) may be administered at a dose of 0.2 to 0.4 mg/kg IV q6–8h. Because it is a dopamine antagonist, do not use it concomitantly with dopamine.

• Alternatively, administer chlorpromazine (Thorazine) at a dose of 0.25 to 0.5 mg/kg IV or IM q6–8h. Because chlorpromazine may cause hypotension and decrease renal perfusion, avoid using it in patients that are dehydrated. Do not combine chlorpromazine and metoclopramide as this can potentiate neurologic side effects.

• Refer to Chapter 67 for other recommendations for treating gastritis and the control of vomiting.

Monitoring Patients

The objectives of monitoring patients are to evaluate response to treatment, avoid potential complications, and help establish a prognosis. Patients generally are monitored more frequently during initial treatment or when life-threatening complications such as severe metabolic acidosis, oliguria, or hyperkalemia exist and less often when there is improvement or stabilization of the patient’s condition. Parameters that are evaluated include hydration status, body weight, urine volume, and laboratory values.

• Record body weight and hydration status 2 to 4 times daily. Clinical estimation of hydration status and fluid losses can be inaccurate. Once a patient is rehydrated, rapid changes in body weight generally reflect net fluid losses or gains and signal the need for a change in the rate of fluid administration.

• Measure hematocrit and total protein values at the end of rehydration and then at minimum daily to help evaluate hydration status.

• Measure serum chemistries and electrolytes at the end of rehydration and then at minimum daily for the first 4 to 7 days.

• Monitor blood gas values or total CO₂ and serum potassium several times daily if severe metabolic acidosis or hyperkalemia exists.

• To prevent overhydration, monitor changes in central venous pressure in patients with cardiac disease or persistent oliguria. In addition, a system of measuring “ins” and “outs” helps guide fluid therapy in these patients (see Chapter 5).

• Place an indwelling urinary catheter in patients that appear to have anuria or oliguria after rehydration. This helps determine the need for measures to stimulate urine production and guides fluid therapy to prevent overhydration.

Treatment of Underlying Causes of ARF

Leptospirosis

• Administer penicillin (20,000–40,000 U/kg IV q12h) or ampicillin (22 mg/kg IV q8h) initially. When vomiting resolves, administer doxycycline (5 mg/kg PO q12h) for 2 weeks to eliminate the carrier state of leptospirosis.

Ethylene Glycol (Antifreeze) Toxicosis

If a patient is presented within 6 hours of ingesting ethylene glycol, induce vomiting, lavage the stomach, and administer activated charcoal. If it has been less than 24 hours since ingestion, administer agents to slow conversion of ethylene glycol to its toxic metabolites. Unfortunately, most patients with ethylene glycol intoxication are presented after ARF develops and the follow-ing treatments are not effective. Remember, not all antifreeze products are ethylene glycol. Products containing propylene glycol are available and are less toxic. If in doubt as to which was consumed, treat for ethylene glycol exposure.

4-Methylpyrazole

• 4-Methylpyrazole (5%) inhibits alcohol dehydrogenase and does not cause central nervous system depression like ethanol. It is the preferred treatment for ethylene glycol intoxication in dogs.

• Administer 0.4 ml/kg IV initially, then 0.3 ml/kg IV at 12 and 24 hours after ingestion, and then a final dose of 0.1 ml/kg IV at 36 hours after ingestion.

• 4-Methylpyrazole is not effective for treatment of ethylene glycol intoxication in cats at dosages administered to dogs and therefore is not generally recommended. There is some evidence to suggest that when 4-methylpyrazole is administered 3 hours after ingestion of ethylene glycol it is safe and effective at preventing renal failure in cats. The dosing schedule is 125 mg/kg IV initially followed by 31.25 mg/kg at 12, 24, and 36 hours after ingestion.

Prevention

Because of expensive treatment and a guarded prognosis, make every effort to prevent ARF whenever possible.

• Warn owners about the danger of ethylene glycol if their pet lives outdoors.

• Do not use nephrotoxic drugs unless absolutely necessary (use enrofloxacin instead of aminoglycosides for severe gram-negative infections). If a nephrotoxic drug must be used, make sure the patient is well hydrated prior to treatment. Monitor serum drug concentrations, biochemical parameters, and urinalyses.

• Older patients often have chronic renal disease and are very susceptible to acute renal injury associated with dehydration or hypotension. Avoid stress and make sure the pet has access to fresh water at all times. Tell owners to avoid administering over-the-counter pain medications such as aspirin or ibuprofen. If general anesthesia is planned, administer IV fluids before and during anesthesia to maintain renal perfusion.

CHRONIC RENAL FAILURE

CRF is a syndrome characterized by inability of the kidneys to perform excretory, regulatory, and synthetic functions due to a loss of nephrons over a period of months to years. Loss of excretory function causes retention of urea nitrogen, creatinine, phosphorus, and other substances that are eliminated by glomerular filtration. Decreased ability of the kidneys to regulate fluid, electrolyte, and acid-base balance causes polyuria and/or polydipsia, hypokalemia, and metabolic acidosis, as well as other abnormalities. Failure of the kidneys to synthesize erythropoietin and calcitriol causes non-regenerative anemia and renal secondary hyperparathyroidism, respectively.

Etiology

Some breeds are predisposed to development of CRF due to congenital or familial renal disease; however, most dogs and cats with CRF are older and have acquired disease. Although many disorders may predispose to development of CRF in middle-aged to older patients, an underlying cause often is not identified. Regardless of the inciting cause, CRF tends to be a progressive and irreversible disorder.

• Congenital and familial diseases that cause CRF in dogs and cats are listed in Table 77-4.

• Infectious and inflammatory disorders may cause glomerular or tubulointerstitial damage that progress to CRF. Immune-mediated glomerular injury (e.g., glomerulonephritis) secondary to infectious or inflammatory diseases often progresses to cause CRF, especially in dogs. Tubulointerstitial inflammation associated with pyelonephritis, leptospirosis, or feline infectious peritonitis may progress to cause CRF.

• Amyloidosis may cause CRF secondary to deposition of amyloid in glomeruli or in the renal medulla.

• Neoplasia of the kidneys infrequently causes CRF. Renal lymphoma in cats is the most common neoplastic cause of CRF.

• Nephrotoxic substances (drugs, toxins, hypercalcemia) usually cause ARF; however, CRF may persist after recovery from the acute insult.

• Hyperthyroidism in cats is often associated with CRF. Although the relationship is not yet fully understood, renal arteriolar hypertension is thought to play a role (see Chapter 31).

• Idiopathic glomerular or tubulointerstitial disease is the most common cause of CRF in dogs and cats. Despite thorough diagnostic evaluation, most patients do not have evidence of an inciting cause of renal injury.

Table 77-4 BREEDS WITH CONGENITAL OR FAMILIAL RENAL DISEASE

Breed	Renal Disease
Abyssinian cat	Renal amyloidosis
Basenji	Renal tubular dysfunction
Beagle	Unilateral renal agenesis, renal amyloidosis
Bernese mountain dog	Glomerulonephritis
Cairn terrier	Polycystic renal disease
Cocker spaniel	Hereditary nephritis
Doberman pinscher	Glomerulonephritis
Domestic longhaired and Persian cats	Idiopathic polycystic kidney disease
English foxhound	Renal amyloidosis
Lhasa apso	Renal dysplasia
Norwegian elkhound	Tubulointerstitial fibrosis
Pembroke Welsh corgi	Telangiectasia (idiopathic renal hematuria)
Samoyed	X-linked nephritis
Shih Tzu	Renal dysplasia
Soft-coated wheaten terrier	Renal dysplasia, protein-losing glomerulopathy