Renal dysplasia in dogs: developmental kidney disease

Overview

Renal dysplasia is a developmental abnormality of kidney tissue structure. Glomeruli, the filtering structures, and renal tubules may remain immature for the animal's age. Visible kidney disease symptoms may take months or years to appear. Kidney damage that has become chronic is irreversible.

Developmental abnormalities differ: in hypoplasia, a smaller-than-normal kidney contains normally formed functional units. In agenesis, a kidney is entirely absent. In polycystic kidney disease, numerous cysts replace normal tissue. These are different abnormalities from renal dysplasia itself.

Renal dysplasia may affect one or both kidneys. With one-sided disease, the opposite kidney usually enlarges to compensate for reduced function. External structural changes and kidney function do not always correspond closely.

Causes

Maturation of the kidney's functional units may proceed unevenly. Small capillaries in immature glomeruli may remain underdeveloped. Fibrous tissue can form later. Inflammatory changes may also develop around renal tubules.

Inherited susceptibility is possible, but the same gene variant may not underlie disease in every breed. Infection, toxins or urine reflux affecting a developing kidney can also disrupt development. The disorder may arise before birth or during the neonatal period. Renal dysplasia has also been found in puppies infected with herpesvirus.

Canine kidneys continue developing during the first 3 months after birth. Some affected dogs have clinically healthy parents. Family relationships in Boxers are consistent with recessive inheritance, but a more complex pattern is also possible.

Risk factors

Renal dysplasia is more common in Golden Retrievers than in other breeds on average. Early-onset kidney disease associated with renal maldevelopment has also been identified in Boxers. Early kidney disease in a family is a reason to investigate relatives' kidney function too.

Uraemia is usually recognised between 6 months and 2 years of age in renal dysplasia. However, disease may already exist before clear symptoms. A nine-patient Boxer group consisted entirely of females, but this may have been chance. It is not evidence that only females are affected.

Typical symptoms

You may notice changes such as:

• A clear increase in drinking.

• More urine than usual.

• Reduced appetite.

• Weight loss and becoming thin.

• Vomiting.

• Becoming quieter than usual.

• Unusually bad breath.

• A puppy falling behind expected growth.

Symptoms resemble those of other chronic kidney diseases. Advanced disease can cause mouth ulcers. Diarrhoea may also occur. Anaemia can increase tiredness and weakness.

Of 9 Boxers with renal maldevelopment, 6 had intermittent vomiting. Slow growth was apparent in 3. Visible symptoms in early chronic kidney disease may be very mild.

Complications and consequences

Damaged kidneys lose the ability to concentrate urine, increasing dehydration risk. Advanced disease may cause anaemia through a shortage of erythropoietin. High blood pressure can occur at any stage of chronic kidney disease. It can damage the retina, central nervous system and heart.

Young dogs may rarely develop kidney-related bone disease as an end-stage complication. The jawbones can then become flexible. Loose teeth may also be associated with this bone disorder. Pathological fractures can occur too.

In 9 Boxers with severe kidney disease associated with maldevelopment, median age at euthanasia was 16 months, ranging from 6–79 months. Their chronic kidney disease had been diagnosed before 1 year of age. A mildly affected dog may remain clinically symptom-free or develop disease only as an adult.

Blood phosphorus may rise as kidney function declines. Increased body acidity and disturbed potassium balance are other possible consequences. Potassium may be low, normal or mildly increased depending on factors such as nutrition and medication.

Diagnosis at the vet

Investigating kidney function

Breed and age at symptom onset contribute to suspicion. Urinalysis, blood counts and biochemistry investigate the effects of kidney disease. Creatinine changes are also assessed against previous results. An upward trend can matter even within the reference range.

Dilute urine in a dehydrated dog suggests an inadequate ability to conserve water. Classification of urinary protein loss is preferably based on at least 2 samples collected over at least 2 weeks. Management of calcium balance assesses ionised calcium specifically, rather than total calcium.

Monitoring SDMA helps detect reduced kidney filtration. Urinary protein loss is measured with the urine protein-to-creatinine ratio, or UPC. Blood pressure is also measured. Urine culture helps investigate concurrent bacterial infection.

Imaging and tissue sampling

Ultrasound can examine kidney size and tissue structure. Normal size does not rule out maldevelopment. Ultrasound changes consistent with dysplasia also occur in other kidney diseases. The diagnosis itself is confirmed with a kidney tissue sample.

A pathologist looks for structures inappropriate for the animal's developmental stage. Tissue sampling may be considered particularly in a young dog with chronic kidney disease. Biopsy is not recommended in advanced stage 4 disease in the same way as in stages 1–3. Chronic kidney disease is staged in a stable, adequately hydrated dog using at least 2 sets of measurements.

In the nine-dog Boxer group, 7 had kidneys of normal size and shape. Two were considered slightly smaller than normal. All had a less distinct boundary between the renal cortex and medulla than usual.

Samples may also contain foetal duct structures or atypical tubular epithelium. At least 100 glomeruli have been proposed for assessment of a sufficiently large sample. Assessing the whole structure of the renal cortex is also important.

Limitations of genetic testing

Nineteen different DNA combinations in the COX-2 region were found in 152 dogs free from renal dysplasia. Tissue examination confirmed absence of dysplasia in some healthy dogs. These DNA variants alone cannot reliably identify the disease.

Treatment

Supportive care and monitoring

The vet tailors treatment to the kidney disease stage and your dog's response. Early care focuses on slowing progression. Later, symptom relief and quality of life take greater priority. Veterinary fluid treatment corrects dehydration when needed.

Anti-sickness medicines may treat nausea and vomiting. Appetite stimulants can help with loss of appetite. Inadequate intake may require a feeding tube. High blood pressure can be treated with antihypertensive medicines. Drugs acting on the renin–angiotensin system can reduce kidney protein loss.

Creatinine and electrolytes, particularly potassium, are also monitored during blood pressure treatment. Once high blood pressure is stable, follow-up continues at least every 3 months. Kidney-related anaemia can be treated with medicines supporting red cell production or a blood transfusion.

Blood pressure is lowered gradually and sustainably to avoid making it too low. If it has already caused organ damage, treatment starts without waiting for further evidence of persistent hypertension.

Anaemia treatment is recommended when haematocrit, the proportion of blood made up of red cells, falls below 30%. It is also recommended for persistent renal anaemia with a haematocrit of 30–35%. Factors such as infection or frequent blood sampling are investigated as possible contributors.

Dehydration is corrected before starting certain medicines affecting blood pressure and protein loss. Otherwise, kidney filtration may decline suddenly. Preventive stomach-protecting medication is not recommended for every dog with kidney disease. Uraemic stomach ulcers are rare in dogs.

Nutrition during growth

A growing puppy needs an individual nutrition plan for both kidney disease and growth. Enough protein is needed for growth. Excessive protein restriction can cause muscle loss. Too little calcium or phosphorus can disrupt skeletal development.

The diet should be complete and support an ideal weight during growth. Once growth ends, protein and phosphorus targets can be adjusted to adult needs. An adult kidney diet restricts phosphorus and provides moderate amounts of good-quality protein. A phosphate binder may be needed if diet alone does not control blood phosphorus.

During phosphate binder treatment, blood calcium and phosphorus are checked every 4–6 weeks until stable, then every 12 weeks. Excessively high blood calcium is avoided during treatment.

Weight and muscle loss may progress particularly in advanced kidney disease. Adequate intake may require assisted feeding, which can also support hydration and medicine administration.

Treatable concurrent conditions

Concurrent bacterial kidney infection, or pyelonephritis, is investigated and treated. Ureteral obstruction is another treatable cause investigated with imaging.

Prevention

Examining affected dogs' relatives may identify early kidney disease. Some Cairn Terrier breed-club guidance excludes dogs with renal dysplasia from breeding. The same guidance also recommends excluding an affected dog's offspring, parents and littermates.

The investigated COX-2 DNA variants also occur in dogs free from kidney disease. They have not been established as reliable markers of renal dysplasia risk. Identifying mild, symptom-free cases can be difficult.

Absence of symptoms alone does not identify every renal dysplasia case in breeding dogs. Early clinical kidney assessment is particularly justified in a Boxer family with early-onset protein-losing kidney disease.

Important for dog owners

Keep fresh water available at all times. Wet food and adding water to food may support fluid intake. Monitor food intake, weight, muscle condition and overall nutritional status. Not every dog with kidney disease needs subcutaneous fluids.

Tell the vet about every medicine, as some can harm the kidneys. Include treats and supplements in nutritional assessment. Some medicines eliminated through the kidneys may accumulate as disease progresses. Report sudden urinary symptoms too, as bacterial infection can worsen chronic kidney disease.

Frequently asked questions

Can renal dysplasia start only in adulthood?

It is a developmental disorder even when symptoms appear later. A mildly affected dog may develop kidney failure only as an adult or remain clinically symptom-free. However, uraemia is usually identified between 6 months and 2 years of age.

Does a routine blood test detect it?

Blood tests can show declining kidney function. However, they do not identify the tissue structure characteristic of dysplasia. Diagnosis relies on a kidney tissue sample. Urinalysis and ultrasound add to the investigation. Blood pressure is also measured to assess risks associated with kidney disease.

Should a puppy's protein intake be reduced straight away?

A growing puppy needs enough protein for growth, while excess is avoided because of kidney disease. Excessive restriction can cause muscle loss. Calcium and phosphorus must also meet skeletal development needs. Nutritional targets change after growth ends to match adult requirements.

Can a genetic test identify the disease?

COX-2 DNA variants linked to renal dysplasia are also found in healthy dogs. Finding these variants therefore does not confirm renal dysplasia. Uncertain inheritance also highlights the importance of family history and clinical investigations. A symptom-free relative may need clinical kidney assessment before breeding decisions too.

Can a dog with kidney disease feel well?

In early chronic kidney disease, a dog may have few or no visible symptoms. Treatment aims to preserve remaining function and reduce symptoms. During follow-up, care is adjusted according to the dog's response.