A review of the renal system and diurnal variations of renal activity in livestock

Kidneys are the main organs regulating water-electrolyte homeostasis in the body. They are responsible for maintaining the total volume of water and its distribution in particular water spaces, for electrolyte composition of systemic fluids and also for maintaining acid-base balance. These functions are performed by the plasma filtration process in renal glomeruli and the processes of active absorption and secretion in renal tubules, all adjusted to an 'activity-rest' rhythm. These diurnal changes are influenced by a 24-hour cycle of activity of hormones engaged in the regulation of renal activity. Studies on spontaneous rhythms of renal activity have been carried out mainly on humans and laboratory animals, but few studies have been carried out on livestock animals. Moreover, those results cover only some aspects of renal physiology. This review gives an overview of current knowledge concerning renal function and diurnal variations of some renal activity parameters in livestock, providing greater understanding of general chronobiological processes in mammals. Detailed knowledge of these rhythms is useful for clinical, practical and pharmacological purposes, as well as studies on their physical performance.     

Strategies for management of acute renal failure.

Acute renal failure (ARF) is often defined as the sudden inability of the kidneys to regulate water and solute balance. ARF may be more broadly defined as rapid deterioration of renal function resulting in the accumulation of nitrogenous wastes such as urea and creatinine. Clinically, oliguria is defined as urine flow of less than 2 mL/kg/h and anuria has no measurable urine production. In animals, the most common cause of ARF is nephrotoxicity; ischemia ranks second, with interstitial and glomerular diseases following.     

Diagnosis and treatment of avian renal disease.

Reports on the incidence of renal disease in the avian patient vary,but renal disease is common in poultry and birds of prey. Clinical renal disease is probably under-recognized in the companion bird,with the notable exception of renal tumors in the budgerigar (Melopsittacusundulatus). Diagnosis of renal disease may rely on the identification of consistent clinical signs, clinical pathology, survey radiographs, and laparoscopic evaluation and biopsy of the kidneys.Treatment of avian renal disease relies on supportive care such as fluid therapy and nutritional support. Other treatments vary with the underlying cause and the clinical picture but may include systemic antibiotics, diuretics, parenteral vitamin A, and agents to lower uric acid levels such as allopurinol.     

Review of the pathophysiology of alterations in potassium homeostasis

The 2 interrelated systems of external and internal balance that regulate potassium homeostasis must function properly if normal plasma potassium concentration and total body potassium content is to be maintained. Should external balance fail, with renal or gastrointestinal wasting of potassium, hypokalemia with depletion of total body potassium may result. In the absence of this type of potassium wasting, hypokalemia most often is caused by redistribution, with potassium moving from the extracellular-fluid into cells and total body potassium content remaining unaltered. Likewise, factors regulating internal balance may redistribute potassium from cells into the extracellular fluid and cause hyperkalemia, but with normal total body potassium content. Should the kidneys or urinary system fail to excrete potassium, hyperkalemia with an increase in total body potassium content would result.     

Managing fluid and electrolyte disorders in renal failure.

Because of the role of the kidneys in maintaining homeostasis in the body, kidney failure leads to derangements of fluid, electrolyte, and acid-base balance. The most effective therapy of a uremic crisis is careful management of fluid balance, which involves thoughtful assessment of hydration, a fluid treatment plan personalized for the specific patient, repeated and frequent reassessment of fluid and electrolyte balance, and appropriate changes in the treatment plan in response to the rapidly changing clinical situation of the patient that has renal failure. Disorders of sodium, chloride, potassium, calcium, and phosphorus are commonly encountered in renal failure and may be life threatening. Treatment of metabolic acidosis and nutritional support are frequently needed.     

A review of phosphorus homeostasis and the impact of different types and amounts of dietary phosphate on metabolism and renal health in cats

Elevated concentrations of serum phosphate are linked with progression and increased case fatality rate in animals and humans with chronic kidney disease. Elevated concentrations of serum phosphate can be a risk factor for development of renal and cardiovascular diseases or osteoporosis in previously healthy people. In rodents, an excess intake of dietary phosphorus combined with an inverse dietary calcium : phosphorus ratio (<1 : 1) contributes to renal calcification. Renal injury also has occured in cats fed experimental diets supplemented with highly soluble phosphate salts, especially in diets with inverse calcium : phosphorus ratios. However, not all phosphorus sources contribute similarly to this effect. This review, which focuses on cats, summarizes the published evidence regarding phosphorus metabolism and homeostasis, including the relative impact of different dietary phosphorus sources, and their impact on the kidneys. No data currently shows that commercial cat foods induce renal injury. However, some diets contain high amounts of phosphorus relative to recommendations and some have inverse Ca : P ratios and so could increase the risk for development of kidney disease. While limiting the use of highly soluble phosphates appears to be important, there are insufficient data to support a specific upper limit for phosphate intake. This review also proposes areas where additional research is needed in order to strengthen conclusions and recommendations regarding dietary phosphorus for cats.     

Water transport in the kidney and nephrogenic diabetes insipidus

Nephrogenic diabetes insipidus is caused by an inability of the kidney to concentrate urine despite adequate concentration of vasopressin in blood and is characterized by polyuria, polydipsia, and hyposthenuria in the presence of plasma hyperosmolality. Nephrogenic diabetes insipidus is the result of defects in water homeostasis in the kidney. Nephrogenic diabetes insipidus occurs when the kidneys cannot or do not respond to vasopressin. There are 2 categories of nephrogenic diabetes insipidus. Congenital nephrogenic diabetes insipidus is a rare, inherited, irreversible cause of polyuria and polydipsia in humans that is even rarer in animals. Acquired nephrogenic diabetes insipidus is more common and is often secondary to illness or medication that interferes with the action of vasopressin in the renal tubules. Unlike congenital nephrogenic diabetes insipidus, acquired or secondary nephrogenic diabetes insipidus is often reversible with correction of the associated or causative problem.     

Epizootiology, pathology, and microbiology of an outbreak of urolithiasis in chickens

An outbreak of urolithiasis that doubled the annual mortality rate of chickens in a large flock of table-egg-layers is described. Despite the presence of a large unilateral urolith and/or severe renal atrophy, the layers often maintained active egg production and apparent homeostasis until a small urolith blocked the ureteral flow from the contralateral kidney. This terminal episode appeared to produce acute obstructive renal failure, rapidly developing visceral gout (visceral urate deposition), uremia, and death. The atrophy observed appeared to be acquired and progressive. Histologic features in the kidneys were acute to chronic glomerulonephritis, interstitial nephritis, and pyelonephritis. Epizootiologic and microbiologic studies indicated that a combination of infectious and noninfectious mechanisms may have been involved. Causative roles for calcium-phosphate imbalance, infectious bronchitis (IB), Newcastle disease (ND), and adenovirus or reovirus infections could be neither excluded nor confirmed. Contributory factors may have been spray ND-IB and other vaccinations of 15-week-old ND-IB-susceptible pullets, water deprivation, shipping stress, Mycoplasma synoviae infection, immune complex disease, and mycotoxins.     

Hemolytic-uremic syndrome in a postpartum mare concurrent with encephalopathy in the neonatal foal.

A postpartum mare and foal were presented for evaluation of fever and lethargy in the mare. The mare was diagnosed with endometritis and initially responded well to treatment. On the second day of hospitalization, the mare developed renal insufficiency characterized by oliguria, azotemia, hemolysis, and thrombocytopenia. Concurrently, the foal developed rapidly progressive central nervous system signs culminating in refractory seizures. Both animals failed to respond to treatment and were euthanized. Thrombotic microangiopathy involving glomeruli was evident on microscopic examination of the mare's kidneys. Microscopic evidence of brain edema was the principal postmortem finding in the foal. No specific etiology was confirmed in either case. Notably, Escherichia coli 0103:H2 was isolated from the mare's uterus and the gastrointestinal tracts of both animals. To the authors' knowledge, this is the first report in which an organism implicated as a cause of hemolytic-uremic syndrome was isolated from an animal with clinical signs and postmortem findings consistent with the disease.     

Abnormal development of nephrons in claudin-16-defective Japanese black cattle

The kidneys of 37 Japanese Black calves aged 2 to 65 months diagnosed with Claudin 16 (CL-16) defect by the DNA-based test were examined pathologically. The animals exhibited clinical symptoms such as growth impairment, renal failure, overgrowth of hooves, and anemia at a young age. There was no correlation between the time of onset and age. Kidney weights relative to body weight were similar to those in normal animals, but both kidney net weights and size were reduced due to atrophy in animals that showed severe renal dysfunction. Histopathological examination of the kidneys showed reduction in the number of glomeruli, compensatory hypertrophy of glomeruli and tubules, and glomerular and tubular atrophy accompanied by interstitial fibrosis and lymphocytic infiltration. Glomeruli were clearly less in number in the kidneys of CL-16-defective animals than those of normal animals even in the cases with mild lesions. A small number of immature glomeruli and tubules were also detected, suggesting that there were fewer nephrons developed at birth in CL-16-defective animals. It was suggested that a defect of the CL-16 gene is involved in the "abnormal development of nephrons". Immunohistopathological examination of the kidneys showed that the epithelium of thick ascending limb of Henle was stained with anti-CL-16 antibody in the control animals, but not in the affected animals, suggesting a defect of CL-16 in the epithelium of renal tubules in the affected animals.     

Congenital and inherited renal disease of small animals.

Congenital renal diseases are present at birth and may be determined genetically; familial renal disorders occur in related animals with a higher frequency than would be expected by chance, and frequently are inherited. The most common familial disorders in cats and dogs include renal amyloidosis, renal dysplasia, polycystic kidneys, basement membrane disorders, and tubular dysfunction (Fanconi's syndrome). This article alerts the veterinarian to commonly observed congenital and hereditary conditions of the kidneys in small animals.     

Pathological changes of renal tubular dysplasia in Japanese black cattle

Pathological studies were conducted on 91 Japanese Black cattle with a hereditary disease which induced growth retardation, long hooves and renal failure. In calves one to two months old, no gross abnormalities were observed in the kidneys, but microscopical examinations revealed immature epithelia which were arranged irregularly and not attached to the basement membranes in some proximal tubules. In animals three to 36 months old, the kidneys had shrunk perceptibly and had grey-white radial streaks; microscopically they showed severe interstitial fibrosis with round-cell infiltration in the outer zone of the medulla and cortex, and reductions in the numbers of glomeruli and tubules. In the fibrotic areas there were immature epithelia with an irregular arrangement, and the basement membrane of the tubules was thickened. It was concluded that renal tubular dysplasia was the primary lesion of the disease, and that interstitial fibrosis and reductions in the numbers of nephrons were secondary lesions.     

Ultrasonographic Features of the Chinchilla (Chinchilla lanigera) Kidney

Nine healthy chinchillas (Chinchilla lanigera) were used to characterize the ultrasonographic size and anatomical structure of the kidneys. Sonographic evaluations were performed with the aid of a 12-MHz linear probe. Kidney measurements included total width and length, total organ area, cortex and medullary thickness, and width and length of the renal pelvis. Based on the results of this study, normal chinchilla kidneys are located retroperitoneally, with the right kidney in a more cranial location than the left. Statistical analysis showed that measurements were similar between contralateral kidneys and between sexes. Chinchilla kidneys have a single papilla and a wider renal pelvis compared with the renal pelvis of dogs and cats. Moreover, chinchilla kidneys have a longer medullary area. The data herein may aid diagnosis of renal disease in chinchillas, avoiding misinterpretations of ultrasonic findings involving the kidneys of this species.     

Change in intrarenal Ghrelin expression in immune complex-mediated glomerular disease in dogs

Ghrelin is a peptide hormone that is mainly produced by the stomach. The kidney is a major source of local ghrelin, and maintaining body fluid balance is considered a critical role of renal ghrelin. However, there are no reports on renal ghrelin in small animal medicine. The present study investigated the intrarenal localization of and change in ghrelin expression in dogs with immune complex-mediated glomerulonephritis (ICGN). Ghrelin immunoreactivity (IR) was observed in the distal tubules of normal kidneys. Ghrelin IR was weak in ICGN kidneys, and the quantitative ghrelin IR score was significantly lower in ICGN kidneys than in normal kidneys. In cases of ICGN, plasma creatinine concentrations showed a positive correlation with the ghrelin IR score.     

Renal regulation of electrolyte and acid-base balance in ruminants

The kidney maintains volume, electrolyte, and acid-base homeostasis. These functions are examined in the ruminant in response to differing dietary intakes and disease states. The consequences of renal disease for these homeostatic processes and the interpretation of urinary excretion data are reviewed.     

Use of 99mTc diethylenetriaminepentaacetic acid for assessment of renal function in dogs with suspected renal disease

The effectiveness of technetium 99m-labeled diethylenetriaminepentaacetic acid (99mTc DTPA) to assess renal function in 13 dogs with suspected renal disease was evaluated. Glomerular filtration rates (actual GFR) were determined on the basis of endogenous creatinine clearance. Predicted GFR were determined by using 99mTc DTPA within 72 hours after the determination of creatinine clearance. The percentage of an IV administered dose of 99mTc DTPA in the kidneys (percentage dose) was determined. Two equations were used to calculate predicted GFR, which were derived from previously reported linear regression analysis of inulin (In) and creatinine (Cr) GFR vs percentage dose 99mTc DTPA in dog kidneys. The correlations of actual GFR vs predicted GFR (In) and actual GFR vs predicted GFR (Cr) were both r = 0.92. The dogs' mean actual GFR was 1.73 +/- 1.35 ml/min/kg. Their mean predicted GFR (In) and predicted GFR (Cr) were 1.92 +/- 1.42 ml/min/kg and 1.85 +/- 1.27 ml/min/kg, respectively. Therefore, 99mTc DTPA can be used with high accuracy as an agent to predict GFR in dogs with suspected renal disease. The procedure for determining GFR by use of nuclear medicine was rapid and noninvasive and appeared to induce little stress in the animals evaluated.     

The role of the kidneys in vitamin metabolism

It is well established that the kidney plays an essential role in regulating the homeostasis of body fluids. Recent studies provided evidence for the kidney to be an important organ for the regulation in the metabolism of both fat (vitamin A, D) and water soluble vitamins (e.g. vitamin B12). This regulation is mediated by glomerular filtration as well as reabsorption and secretion processes of protein-bound vitamins. Vitamin transport proteins such as retinol-binding protein, vitamin D-binding protein and transcobalamin II are filtered in renal glomeruli and subsequently reabsorbed in the proximal tubules by endocytosis from the tubular fluid. Megalin, a scavenger receptor belonging to the LDL receptor family, is probably the most important receptor in this process in the proximal tubule cells. The carrier proteins are degraded in lysosomes whereas the vitamins are probably stored, may become coupled to newly synthesized carriers and secreted at the basolateral plasma membrane. A renal vitamin excretion is observed in dogs and other species of the family Canidae, in form of fat soluble retinol and retinyl esters bound to Tamm-Horsfall protein. This and the high vitamin A concentrations in renal tissue of canines suggest an important role of the kidneys in vitamin A metabolism of these species.     

Changes in the localization of type I, III and IV collagen mRNAs in the kidneys of hereditary nephritic (ICGN) mice with renal fibrosis

Renal fibrotic change, extreme accumulation of extracellular matrix (ECM) components in glomeruli and tubulointerstitum, is one of the characteristic features of ICR-derived glomerulonephritis (ICGN) mice. Decreased degradation of ECMs by matrixmetalloproteinases was demonstrated in kidneys of ICGN mice. To determine the balance between production and degradation of ECMs in kidneys of ICGN mice, we examined expression of mRNAs of ECMs in those. To demonstrate the localization of type I, III and IV collagen mRNAs in kidney sections of ICGN and control ICR mice, in situ hybridization using digoxigenin-labeled oligonucleotide antisense probes for procollagen-alpha(1) (I), -alpha(1) (III) and -alpha(1) (IV) mRNAs, respectively, was performed. Negative or trace expressions of type I and III collagen mRNAs were observed in the kidneys of control mice, but stronger expressions of those were seen in glomeruli and injured renal tubules of the kidneys of ICGN mice. Moderate expression of type IV collagen mRNA was demonstrated in a part of glomeruli and renal tubules of both control and ICGN mice, and no remarkable difference was seen between them. Severe renal fibrosis, extreme accumulation of interstitial type I and III collagens is caused by increased production and decreased degradation in the kidneys of ICGN mice. Thus, the profiles of metabolism between interstitial and membranous collagens may be different in the kidneys of ICGN mice, and excessive production of interstitial collagens may be the dominant cause of renal disease in them.     

NONHUMAN PRIMATE EXCRETORY UROGRAPHY*

Survey radiographs have not accurately identified renal contour or location in nonhuman primates. Excretory urography using 786 to 1193 mg iodinelkg body weight resulted in dense opacification of the renal parenchyma and pelvis. Abdominal compression improved visu- alization of the renal pelvis. Interpretation of the nonhuman primate excretory urogram was compromised by several anatomic characteristics of this animal group. Superimposition of the kidneys on the lateral radiograph limited evaluation of the renal contour. Since the renal pelvis in most species of nonhuman primates does not possess diverticula (as in the dog and cat) or a caliceal system (as in the pig and man), the diagnosis of pyelonephritis or renal mass lesions was difficult. Severe irregularities in the renal contour, size of the renal pelvis, or areas of deficient concentrating ability were identifiable in nonhuman primate excretory urograms, but the diagnosis of small cysts was not possible in smaller nonhuman primates. The presence of a caliceal collecting system in the spider monkey (Ateles sp.) suggests this animal as a potential model for the evaluation of human renal disease.     

Polycystic kidney disease in bull terriers: an autosomal dominant inherited disorder

The prevalence, mode of inheritance and urinalysis findings in Bull Terriers with polycystic kidney disease were assessed by screening 150 clinically normal dogs. The disorder was diagnosed in 39 dogs on the basis of renal ultrasound results and family history of the disease. In equivocal cases confirmation required gross and histopathological renal examination. Necropsy was performed on nine affected dogs and the kidneys from another five affected animals were also examined. Renal cysts were usually bilateral, occurred in cortex and medulla and varied from less than 1 mm to over 2.5 cm in diameter. Cysts were lined by epithelial cells of nephron origin. Abnormal urine sediment and proteinuria were common in affected dogs. The disease appears to be inherited in a highly penetrant autosomal dominant manner.