• chronic interstitial nephritis
• hydronephrosis
• hypercalcemia
• parasites

Chronic interstitial nephritis (CIN) is similar to the term end stage renal disease (ESRD) in that it is a non specific histologic finding on renal biopsy and may be the end result of renal disease of any etiology.

Hydronephrosis

Hydronephrosis is the progressive dilation of the renal pelvis (or pelves if bilateral) resulting in progressive atrophy of renal parenchyma. The cause of hydronephrosis is complete or partial obstruction to urine outflow. Obstruction may be caused by:

• calculi in the renal pelvis or ureter
• neoplastic or inflammatory masses which compress the ureter(s)
• accidental ligation of a ureter during surgery
• blood clot in the renal pelvis
• the ureters can be bilaterally affected by a mass in the trigone of the bladder such as a transitional cell carcinoma.

There is continued production of urine following obstruction and the increased volume and pressure in urinary tract proximal to the obstruction leads to dilation and atrophy of tubules. If obstruction is bilateral and complete, the animal will die of uremia in 3 to 6 days. If obstruction is unilateral with normal function of opposite kidney, there are often no symptoms. The hydronephrotic kidney may be discovered as an incidental finding, years after the event which caused it.

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Hypercalcemia

Hypercalcemia is defined as total calcium > 12 mg/dl in adult dog and > 11 mg/dl in the cat. Total calcium concentrations can be as high as 13 mg/dl in the growing pup and are usually accompanied by phosphorus values as high as 10 mg/dl and elevation of serum alkaline phosphorus. Blood calcium does not fluctuate in the growing cat.

Total calcium = 50% ionized + 40% protein bound + 10% complexed

Elevation or reduction of serum albumin will influence total calcium concentration. Total calcium can be corrected for abnormal albumin concentrations using this formula:

corrected total calcium = serum calcium (mg/dl) - albumin (g/dl) + 3.5

Calcium concentrations less than 14 mg/dl often are "clinically silent" (do not cause clinical signs). Clinical signs which may occur include:

• decreased excitability of gastrointestinal smooth muscle leading to anorexia, vomiting, or constipation
• generalized skeletal muscle weakness
• ventricular fibrillation or other cardiac arrhythmia (not common - may be seen with calcium >18 mg/dl)
• PU/PD

There are several postulated mechanisms for the impairment in renal concentrating ability.

• calcium induced damage to ADH receptors in tubular cells (nephrogenic diabetes insipidus)
• inactivation of adenylate cyclase
• impaired Na or Cl pumping
• mineralization of renal tubular epithelial cells.

Renal injury and azotemia may develop as a result of direct toxicity to renal tubular epithelium and hypercalcemic induced vasoconstriction of renal vessels leading to ischemia.

The list of differential diagnosis for hypercalcemia includes:

• pseudohyperparathyroidism caused by malignant tumors of nonparathyroid origin that produce a parathormone like substance, or an osteoclast activating factor which mobilizes calcium from bone. Tumor types that result in pseudohyperparathyroidism:

  lymphosarcoma
  perirectal tumors of apocrine gland origin
  adenocarcinoma and squamous cell carcinoma of mammary glands
  occasionally other tumor types

• osteolysis by multiple myeloma tumor or primary bone tumors
• primary hyperparathyroidism
• hypervitaminosis D either due to supplementation or intoxication with a house plant (day blooming jasmine) or vitamin D containing rodenticide
• CRF (tertiary hyperparathyroidism)
• hypoadrenocorticism

It is usually not difficult to identify the cause of elevated serum calcium. Pseudohyperparathyroidism due to lymphoma and perirectal tumors are the most common causes of hypercalcemia. Primary hyperparathyroidism occurs infrequently. The history may provide information about possible rodenticide exposure. A physical exam will often disclose enlarged lymph nodes in patients with lymphoma although some forms of lymphoma such as the intestinal form may not have abnormalities detectable by examination. Rectal exam will often detect perirectal tumors, although some can be quite small so careful palpation is necessary. The magnitude of elevation of hypercalcemia, phosphorus level and PTH level can all be used to differentiate between the causes of hypercalcemia.

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This chart, modified from p625, Essentials of small animal medicine, Couto, Nelson, Mosby Publishers, 1992, shows the relative magnitude of elevation or reduction of calcium and phosphorus in various disease states:

• primary = primary hyperparathyroidism
• pseudo = pseudohyperparathyroidism = hypercalcemia of malignancy
• renal = renal disease
• vit D tox = vitamin D toxicity
• nutritional = nutritional hyperparathyroidism
• Addison's = hypoadrenocortisim

Additionally PTH can be measured and is increased in patients with primary hyperparathyroidism and renal failure.

Treatment of hypercalcemia

Treat the underlying cause if possible and hypercalcemia may regress without specific treatment. Sodium chloride diuresis promotes calcium loss in the urine (calciuresis). Diuretics such as furosemide also promote urinary loss of calcium regardless of the cause for hypercalcemia. Thiazide diuretics promote calcium reabsorption and are therefore contraindicated. Glucocorticoids cause calciuresis and decrease the intestinal absorption of calcium. Glucocorticoids will cause lysis of neoplastic lymphocytes and therefore should not be given until a diagnosis has been made. Mithramycin is an anti cancer agent that reduces calcium reabsorption from bone. Calcitonin is quite effective in rapidly lowering serum calcium. Pamidronate is a second generation biphosphonate.  Diphosphonates inhibit osteoclastic bone reabsorption resulting in a reduction in serum calcium.

Parasites of the canine urinary tract

Dioctophyma renale is the giant kidney worm. The principal definitive hosts are wild fish eating carnivores. The prevalence in dogs in the U.S. is low.

The life cycle begins with eggs shed in urine of the definitive host. The eggs are ingested by a crayfish, then the crayfish is eaten by fish or frog. The definitive host is infected when it eats the fish or frog. The larvae penetrate the stomach and enter the abdominal cavity and sometimes kidney. Affected animals are frequently asymptomatic but may show peritonitis and ascites or signs of uremia.

The diagnosis is made by identification of eggs in urine and an enlarged kidney on radiograph. Treatment is a nephrectomy.

Capillaria plica are transmitted by earthworms and localize in the renal pelvis, ureter and bladder. The affected animal is generally asymptomatic. Eggs can be found in the urine. The treatment is albendazole.