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Comparison of 3 techniques for ureteroneocystostomy in cats.

OBJECTIVE: To compare 3 techniques for ureteroneocystostomy in cats. STUDY DESIGN: Experimental surgical study. ANIMALS: Fifteen adult cats. METHODS: Cats (15) had ureteroneocystostomy with ureteronephrectomy of the contralateral kidney: 5 cats had an intravesical mucosal apposition technique (modified Leadbetter-Politano; intravesical-MA group), 5 cats had extravesical ureteroneocystostomy (modified Lich Gregoir) using a simple continuous suture pattern (extravesical-SC group) and 5 cats had an extravesical technique using a simple interrupted suture pattern (extravesical-SI group). Renal function was evaluated by measuring serum creatinine concentration. Ultrasonographic assessment of the kidney and ureteroneocystostomy site was performed the day after surgery, twice weekly for 3 weeks and once weekly for the remainder of the study. Cats were euthanatized 50 days after surgery. The kidney and ureter removed at surgery, the remaining kidney, ureter, ureteroneocystostomy site, and bladder were examined histologically. RESULTS: Two extravesical-SC cats were euthanatized because of azotemia and uroabdomen, and 1 died acutely at day 4 for unknown reasons. In the intravesical-MA and extravesical-SI cats, the serum creatinine concentration increased after surgery, peaking at a mean (+/-SD) of 9.4+/-2.4 mg/dL and 4.9+/-3.3 mg/dL on day 3, and decreasing to 3.4+/-5.7 mg/dL and 1.5+/-0.4 mg/dL on day 7, respectively. The extravesical-SI technique was associated with consistently lower serum creatinine concentrations for the first week after surgery compared with the other techniques. The mean serum creatinine concentration was within the reference range in cats in the intravesical-MA and extravesical-SI groups by days 10 and 5, respectively. Renal pelvic dilatation occurred in all cats but resolved more rapidly in cats after extravesical techniques. There was no significant difference in serum creatinine concentrations or renal pelvic dilation between the intravesical-MA and extravesical-SI techniques. Bladder mass height at the anastomosis site was significantly larger and persisted for longer with intravesical-MA technique. CONCLUSION: An extravesical-SI technique is seemingly the choice for ureteroneocystostomy in cats with undilated ureters. Renal pelvic dilation on ultrasound examination should be expected after ureteroneocystostomy in cats. CLINICAL RELEVANCE: An extravesical ureteroneocystostomy technique using a simple interrupted pattern for anastomosis should be considered in cats undergoing renal transplantation.

Animals↗

Lithium treatment and kidney function. A survey of 237 patients in long-term treatment.

Kidney function has been examined in 237 patients who in the autumn of 1977 were in lithium treatment at the Psychiatric Hospital in Risskov, most of them as outpatients. The average age was 42 years. The patients had been given lithium treatment for 0.5-17 years, mean duration 5 years. The mean lithium dosage was 33 mmol/day and the mean 12-hour serum lithium concentration 0.85 mmol/l. Glomerular filtration rate was assessed through determination of 24-hour creatinine clearance and serum creatinine, in some cases iothalamate clearance. Water excretion was assessed through determination of 24-hour urine volume and in some cases urine osmolality after 26 hours of fluid deprivation. Creatinine clearances, serum creatinine concentrations, and urine volumes were subjected to multiple regression analysis with various clinically relevant predictor variables. Affection of glomerular filtration rate was only moderate and progressed slowly. The data indicate that the risk of renal insufficiency and terminal azotemia is remote even when lithium is given for many years. A large number of the patients had altered water excretion with polyuria or lowered urine concentrating ability or both. Due to the extra fluid loss these patients are apt to develop dehydration, and they may then be in danger of lithium poisoning. We hypothesize that lithium-induced changes of kidney function may become less frequent and less pronounced if patients are maintained at serum lithium levels somewhat lower than those employed in the group studied here. We recommend careful monitoring of serum lithium levels, regular control of kidney function, and extra caution when physical illness or additional drug treatment may lead to disturbance of fluid and electrolyte balance.

Adult↗

Review of exertional rhabdomyolysis and a case in a rhesus monkey (Macaca mulatta).

This is the first confirmed report of exertional rhabdomyolysis in a non-human primate. The monkey was singly housed and presented with anorexia and reluctance to move. There was no external evidence of trauma. Clinicopathologic findings included mild azotemia, marked elevation in serum creatine phosphokinase (CPK), alanine aminotransferase, aspartate aminotransferase, and myoglobinuria. Two days post-incident, the peripheral skeletal muscle had marked multifocal myonecrosis and fibrillar disruption without an inflammatory reaction. Treatment included diuresis and pain relief, and urinary output was monitored. The monkey recovered over the next two weeks. The major significance of skeletal muscle damage is the potential of released myoglobin to cause acute renal failure in the presence of other co-factors such as hypovolemia, acidosis, or ischemia. CPK levels can be highly variable and are inconsistent with the degree of muscle damage; however, CPK is thought to be the most sensitive enzyme marker for muscle necrosis. Because of the potential life-threatening sequelae, exertional rhabdomyolysis should be included as a differential diagnosis when similar clinical and pathological signs are observed.

Alanine Transaminase↗

Type 4 renal tubular acidosis (sub-type 2) associated with idiopathic interstitial nephritis.

An 18-month-old girl presenting with anorexia and failure to thrive, was referred for adenoidectomy. Arterial hypertension was discovered on physical examination. Laboratory results revealed hyperkalaemic, hyperchloraemic, metabolic acidosis, with slight azotemia. Urinary aldosterone excretion and plasma renin were decreased. Renal biopsy showed idiopathic interstitial nephritis. The diagnosis of type 4 renal tubular acidosis, sub-type 2, i.e. primary hyporeninaemic secondary hypoaldosteronism was proposed. According to our knowledge, this disease has not previously been reported in young children, but is well known in azotaemic adults. We therefore propose the inclusion of this uncommon renal disease in the differential diagnosis of failure to thrive in childhood.

Acidosis, Renal Tubular↗

Autologous immune complex nephritis and DOCA-NaCl load: a new model of hypertension.

In order to explore immunological features of hypertension, we studied autologous immune complex nephritis (Heymann nephritis) combined with DOCA-NaCl treatment. This combination resulted in hypertension and increased heart weight whereas DOCA-NaCl treatment alone induced only a slight elevation of blood pressure and a moderate increase in heart weight. Nephritic rats without DOCA-NaCl load remained normotensive, their heart weights being comparable to those of controls. This new model of hypertension was neither characterized by azotemia nor by reduced renal excretory capacity. Hypertension was not renin-angiotensin-dependent. DOCA-NaCl treatment accelerated the development of proteinuria. In the hypertensive rats, systolic blood pressure to daily urinary protein excretion. Renal histopathology revealed changes resembling those of malignant nephrosclerosis. Immunohistology and electron microscopy showed a typical membranous glomerulonephritis in all immunized animals. It was concluded that immune complex disease of the Heymann nephritis type may interfere with normal hemodynamic adaptation to hypervolemic sodium load, resulting in hypertension.

Animals↗

Different blood pressure response to DOCA-NaCl treatment in autoimmune and N,N'- diacetylbenzidine-induced nephropathies.

In order to explore the effect of immunologically-induced nephropathy versus a non-immunological model on development of hypertension, rats with either Heymann nephritis or N,N'-diacetylbenzidine (N,N'-DAB)-induced nephropathy were subjected to DOCA-NaCl treatment. Hypertension developed during DOCA-NaCl treatment in Heymann nephritic rats but not in rats wih N, N'-DAB nephropathy, despite similar degrees of proteinuria and other features of nephrosis. There were no signs of different fluid balance, either. Azotemia did not ensue. Histology and immunohistology showed membranous glomerulonephritis in Heymann nephritic rats whereas glomerular epithelial cell alterations without immune deposits along the glomerular capillary walls were seen in rats with N, N'-DAB nephropathy. The type of renal damage or factors mediating such damage appear to be important determinants for the hypertensive response of Heymann nephritic rats to DOCA-NaCl treatment.

Animals↗

Ultrasound-assisted diagnosis of renal dysplasia in a 3-month-old Quarter Horse colt.

A 3-month-old foal was presented for correction of bilateral angular limb deformities. Azotemia was detected as an incidental finding. Small, misshapened, hyperechoic kidneys with decreased corticomedullary demarcation were noted with ultrasonography. Additionally, the internal renal architecture was abnormal in that the intrarenal vessels and distant collecting system were not clearly seen in either kidney. Ultrasound-guided renal biopsy was suggestive of congenital renal dysplasia, which was later confirmed at necropsy. Clinical, sonographic, and pathologic features of equine renal dysplasia are discussed.

Animals↗

Chronic renal failure associated with nephrolithiasis, ureterolithiasis, and renal dysplasia in a 2-year-old quarter horse gelding.

A 2-year-old quarter horse gelding presented for evaluation of polyuria and polydipsia. Azotemia was detected on serum chemistry profile. Small, misshapen, hyperechoic kidneys with decreased corticomedullary demarcation, hydronephrosis, and a right nephrolith were noted ultrasonographically. The diagnosis of end-stage kidney disease and dysplasia was made histopathologically using ultrasound-guided biopsy. Two ureteroliths were found in the right ureter via cystoscopy, and a nephrolith was seen in the right kidney at necropsy. Clinical, ultrasonographic, and pathologic features of equine urolithiasis and renal dysplasia are discussed.

Animals↗

The nephrotoxicity of Isotropis forrestii in sheep.

Sheep were drenched with a single toxic dose of dried and milled Isotropis forrestii in water. Intoxication resulted in early onset of glycosuria, enzymuria and proteinuria. Terminal gross lesions included pale kidneys and perirenal oedema. Histologically and ultrastructurally the renal lesions were typical of primary nephrotoxicosis, with extensive proximal tubular epithelial necrosis. The tubular damage was sufficient to cause acute primary renal failure, characterised by oliguria, azotemia and failure of urinary concentrating mechanisms.

Animals↗

Nocardial peritonitis in a cat.

OBJECTIVE: To illustrate a successfully managed case of nocardial peritonitis in a cat. DESIGN: Case report. ANIMAL: An 8 year old neutered male Burmese cat presented for nonspecific signs of depression, anorexia, pallor and mild dehydration. Pyrexia, loss of weight and abdominal distension developed despite treatment with amoxycillin-clavulanate and supportive therapy. PROCEDURE: Various medical and surgical procedures were used. RESULTS: Haematology revealed severe inflammatory left shift. Biochemistry showed mild prerenal azotemia. A "ground glass" appearance to the abdomen was seen on radiographs. Fluid collected by abdominocentesis contained "sulphur granules" and had characteristics of a septic exudate. Laparotomy allowed drainage of peritoneal fluid and extensive lavage of the peritoneal cavity. Culture of the fluid revealed Nocardia sp. Sensitivity testing resulted in a change of antimicrobial therapy to trimethoprim-sulphadiazine. CONCLUSION: Response to surgical drainage and change in antibacterial therapy was excellent. No toxic side effects were encountered during the 3 months course of trimethoprim-sulphonamide. The cat made a complete recovery.

Animals↗

Treatment of patients with acute renal failure during Marmara earthquake.

Crush syndrome or traumatic rhabdomyolysis is a serious and epidemic clinical case that develops among casualties of earthquakes or other catastrophic events. Hypocalcaemia is one of the main symptoms that accompanies crush syndrome. It is essential that immediate IV volume replacement treatment be initiated for such patients, which is known to positively affect prognosis and help prevent the development of acute renal failure. Following the earthquake of 17th August 1999 in the north-west of Turkey, 333 casualties were hospitalised in the Medical Faculty of Uludag University. 60 (18%) of these patients [34 males (56.6%) and 26 females (43.4%)] received haemodialysis treatment. The average number of HD sessions received bythe patients was 48. Intermittent HD applied to 44 patients (73.3%) was the preferred method of treatment. Fluid overload and azotemia were the leading indications (76.6%) for dialysis. The lower extremities were mainly injured in these patients [33 (55%)]. Therefore, subclavian catheterisation was preferred in those patients with trauma at this site. 594 (67.1%) HD sessions were applied with limited heparin due to the risk of bleeding. Hypotension in 94 patients (61%) and thrombosis in 60 (45.7%) were the main complications. Of the complications not due to HD, infection in 23 patients (38.3%) was the most significant. 21 patients (35%) were lost during the treatment. It was thanks to the sacrifices and co-operation among national and international medical teams that the mortality rate was low.

Acute Kidney Injury↗

Chronic renal failure, nursing diagnoses and interventions.

Chronic renal failure (CRF) is a clinical condition resulting from a multitude of pathologic processes which lead to derangement and insufficiency of renal excretory and regulatory functions (uraemia). There are normally two million glomeruli in both the kidneys of an adult, which filter an average amount of 120 ml of blood per minute. This filtration is called glomerular filtration rate (GFR). In the case of damaged parenchyma tissues due to renal disease, the filtration rate goes down to 20-30 ml per minute. This is when findings and symptoms of renal failure come about. In the case of a filtration rate less than 10 ml (GFR< 10 ml/min), a patient is understood to have reached the final stage of renal failure. At this stage, fluid and electrolyte balance is disturbed, azotemia increases and systemic manifestations (uraemia) occur (1,2). Renal failure is a condition in which the kidneys cannot fulfil their function of discharging metabolic waste and of maintaining the fluid and electrolyte balance. It can be divided into two groups: acute and chronic. This paper discusses the etiology, pathophysiology and signs and symptoms f CRF as well as the diagnosis and interventions required by nurses. Deficit, nursing priority and intervention are discussed in relation to patient problems.

Disease Progression↗

Potential role of serum inhibitors of erythropoiesis in the anemia associated with infection, renal disease and malignancy in the dog.

Serum from dogs with anemia secondary to infection, malignancy and chronic renal disease was tested for the capacity to inhibit in vitro erythropoiesis. Serum inhibition was found in seven of 10 dogs with infectious diseases, four of 10 dogs with malignant diseases, and two of 10 dogs with chronic renal failure. The results were reproducible with at least three different marrow donor dogs. Serum inhibition did not correlate with decreased packed cell volumes. However, serum inhibition occurred in the two dogs with greatest azotemia suggesting that inhibitors of erythropoiesis are present only in advanced stages of renal failure.

Journal Article↗

Parasitemia in a neonatal bison calf.

A 3-day old female bison calf (Bison bison) was presented in lateral recumbency to the Université de Montréal Veterinary Teaching Hospital. The animal was severely depressed and dehydrated (10%) and died a few hours after admission. Prior to death, blood samples were obtained for CBC, clinical chemistry, and serology tests. Abnormal CBC findings included thrombocytopenia, lymphocytosis, mild monocytosis, and a toxic left shift. Abnormal serum clinical chemistry findings included marked azotemia, hyperphosphatemia, hypernatremia, hyperalbuminemia, hypoglobulinemia, and low gamma-glutamyltransferase activity. Serologic test results for bovine leukosis virus and bovine viral diarrhea virus were negative. Blood smear examination revealed numerous elongated organisms that were tapered at both ends and characterized by an undulating membrane and a long flagellum. The organisms ranged in length from 35 to 40 micro meter, excluding the flagellum, and were identified as Trypanosoma theileri. Postmortem examination revealed that the animal suffered from concurrent mycotic abomasitis and colisepticemia.

Animals↗

Neurologic signs and hyperammonemia in a horse with colic.

A 23-year-old Thoroughbred gelding was referred for the evaluation of acute onset of ataxia and depression, and a 2-day history of fever. On physical examination, the gelding was profoundly depressed and 10-12% dehydrated. The horse appeared very unstable, with a wide-based stance in the hind limbs, severe symmetric ataxia in all 4 limbs, and proprioceptive deficits in both hind limbs. Nasogastric intubation produced 4 L of brown, fetid reflux, and rectal examination revealed mild small intestinal and cecal distention. Hematologic abnormalities included neutropenia with toxic change, compatible with acute inflammation and endotoxemia, and prolonged coagulation times. Serum biochemical abnormalities included prerenal azotemia. metabolic acidosis, and electrolyte abnormalities consistent with enteritis. Blood ammonia concentration was markedly increased (406 micromol/L; reference interval 4-49 micromol/L), however, serum bile acids concentration and hepatic enzyme activities were within reference intervals. Histopathologic examination of a liver biopsy revealed no abnormalities and results of tests for several infectious agents were negative. Clinical signs resolved with correction of the dehydration and electrolyte abnormalities and with antibiotic therapy. The horse was diagnosed with hyperammonemic neuropathy associated with gastrointestinal disease. In such cases, hyperammonemia is caused by increased production of ammonia by organisms in the gastrointestinal tract in combination with increased gut permeability that facilitates ammonia absorption.

Animals↗

The importance of egg protein in reduced protein diets designed for dogs with renal failure.

The effects of two reduced-protein diets and a canine maintenance diet on renal function, nutrition, serum and urine acid-base and electrolyte values, and divalent ion metabolism were compared in Beagle dogs with induced chronic renal failure. Two reduced-protein (18%) diets differed in their protein sources. One 18% protein diet was formulated using egg protein as the only protein source. The other 18% protein diet was formulated using a mixture of animal and vegetable proteins. The 42% protein diet contained a mixture of animal and vegetable protein sources. Results of this study indicate that the egg-based and mixed protein-based diets had similar effects on most clinical and laboratory evaluations in dogs with chronic renal failure. However, the egg protein diet appeared to promote hyperchloremic metabolic acidosis. Both reduced-protein diets were beneficial in reducing azotemia, polyuria, hypermagnesemia, and fractional excretion of phosphorus compared with the 42% protein diet.

Acid-Base Equilibrium↗

Cantharidin toxicosis in horses.

Cantharidin toxicosis in horses has become an increasing problem in certain regions of the United States. Toxicosis occurs when horses ingest alfalfa hay or products that are contaminated with "blister" beetles. Clinical signs may vary from depression to severe shock and death, depending upon the amount of toxin ingested. The most frequently observed signs include varying degrees of abdominal pain, anorexia, depression, and signs suggestive of oral irritation. Many horses make frequent attempts to void urine. Less commonly observed signs include synchronous diaphragmatic flutter and erosions of the oral mucosal surfaces. Clinical laboratory abnormalities suggestive of cantharidin toxicosis include persistent hypocalcemia and hypomagnesemia, development of hypoproteinemia, microscopic hematuria, and mild azotemia with inappropriate urine specific gravity. Chemical analysis for cantharidin is accomplished by evaluation of urine or stomach contents. Treatment of cantharidin toxicosis is symptomatic, but must include removal of toxin source. Gastrointestinal protectants, laxative, intravenous fluids, analgesics, diuretics, calcium gluconate, and magnesium are all included in the treatment regimen. Early and vigorous therapy is imperative if it is to be successful. In horses that remain alive for several days, persistence of elevated heart and respiratory rates and increasing serum creatine kinase concentration are associated with a deteriorating condition. Prevention is aimed at timely harvesting of alfalfa hay. Hay fields should be inspected for the presence of beetle clusters before harvesting. Involved areas of the field should not be harvested.

Animals↗

Primary hypoadrenocorticism in ten cats.

Primary hypoadrenocorticism was diagnosed in ten young to middle-aged cats of mixed breeding. Five of the cats were male, and five were female. Historic signs included lethargy (n = 10), anorexia (n = 10), weight loss (n = 9), vomiting (n = 4), and polyuria (n = 3). Dehydration (n = 9), hypothermia (n = 8), prolonged capillary refill time (n = 5), weak pulse (n = 5), collapse (n = 3), and sinus bradycardia (n = 2) were found on physical examination. Results of initial laboratory tests revealed anemia (n = 3), absolute lymphocytosis (n = 2), absolute eosinophilia (n = 1), and azotemia and hyperphosphatemia (n = 10). Serum electrolyte changes included hyponatremia (n = 10), hyperkalemia (n = 9), hypochloremia (n = 9), and hypercalcemia (n = 1). The diagnosis of primary adrenocortical insufficiency was established on the basis of results of adrenocorticotropic hormone (ACTH) stimulation tests (n = 10) and endogenous plasma ACTH determinations (n = 7). Initial therapy for hypoadrenocorticism included intravenous administration of 0.9% saline and dexamethasone and intramuscular administration of desoxycorticosterone acetate in oil. Three cats were euthanatized shortly after diagnosis because of poor clinical response. Results of necropsy examination were unremarkable except for complete destruction of both adrenal cortices. Seven cats were treated chronically with oral prednisone or intramuscular methylprednisolone acetate for glucocorticoid supplementation and with oral fludrocortisone acetate or intramuscular injections of repository desoxycorticosterone pivalate for mineralocorticoid replacement. One cat died after 47 days of therapy from unknown causes; the other six cats are still alive and well after 3 to 70 months of treatment.

Addison Disease↗