An overwhelming majority of various nephropathies in animals take clinically silent course for a long period of time. But the absence of clinical signs is not the reason for a doctor to make no effort to detect a specific nephrological diagnosis in time and begin therapy before the symptoms of uremia arise. Clinical diagnosis in nephrology, in the majority of cases, is made on the grounds of laboratory examinations of biological fluids blood serum, urine.
However, diverse pathologic changes in renal parenchyma especially glomerular and tubulo-interstitial diseases can lead to very similar changes in the results of laboratory diagnostics at all stages of its development. Rather often some processes in which the condition of renal parenchyma especially at initial phase of pathological process remains normal pre and post-renal RI result in CRI. Nowadays, final diagnosis and institution of complex therapy are possible only on the basis of invasive diagnostic techniques aspiration and puncture biopsies of kidney. A whole number of researches also hold the same opinion.
When defining diagnosis, making optimal therapeutic decisions and medical prognosis the doctor should appeal both functional and morphological data intravital biopsy. Repeated biopsy may be needed for monitoring of clinical behavior of KD or therapy response. Wright et al, These methods of diagnostics, due to the high level of modern medical technologies development are easy to use, low-traumatic and highly informative. Also, Leveille et al. At the same time, value of invasive diagnostics technique in ill and experimental animals and total renal tissue examination after autopsy followed by light and electron microscopy consists in:.
Correct nephrological diagnosis should be made at the earliest possible stages of pathologic process, when medicamentous therapy is the most effective.
In other words, if diagnosis is correct, scientifically grounded and made at an early stage of pathologic process, the doctor has strong reasons to recommend the patient drug therapy including hormonotherapy and dietotherapy for a long period of time from a course of treatment and up to continuous lifelong therapy. The absence of such practice in veterinary nephrology is solely explained by lack of elementary knowledge in this field among the owners of the cats.
Popularization of such knowledge is the task for the veterinary doctors. In — during clinical examinations of cats anamnesis, examinations of biologic fluids, US of abdominal cavity organs in the age from 5 month to 19 years with various health problems, in animals various nephropathies were detected with RI or without it.
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Diagnosis was made according to data of bacterial inoculation of urine, received with by direct urine inoculation method. Taking into consideration the circumstance that the most frequently recorded disorders in cats are various nephropathies, the following tasks were set:. In the period from the year to histomorphological research of kidneys was carried out in cats, died from various diseases or euthanized because of injures or some other pathologies incompatible with life.
Isolated nephritic syndrome was diagnosed in majority of animals. Creatinine level in blood serum was within the normal limit. In the years - , in cats of both sexes aged from 11 months to 18 years, out of the cats taken for the research i. Glomerulonephritis in cats is a group of morphologically heterogenous immune-inflammatory diseases of kidneys which are primary characterized by glomerule dominating lesion and the subsequent involvement of the other kidneys structures into the pathological process. Glomerulonephritis in cats are taking chronic course in overwhelming majority of cases lifelong period.
There is no integrated unified common classification of GN and GP that answer the demands of clinician of different fields, transplantologists and morphologists, up to now. In this review an attempt to synthesize various classifications of GN was made, in order to help vet general practitioner in:.
The key point of aetiological classification of GN is the detection of endogenous or exogenous AG activating agents , which initiate a cascade of immunological responses, which finally by-turn lead to glomeruli lesion. Taking into consideration the fact that GN starts to develop weeks or even month after AG impact and often diagnosed even later , it is very difficult or impossible to determine primary cause sensitization factor in every specific patient. Therefore, more often clinicians have to attribute GN to idiopathic disease.
Probably, one of the leading factors of GN in cats is various low pathogenic viruses , which are constantly, over a lifelong period, persist in organism of the majority of animals latent and chronic infections. Also, there are suppositions that various viral AG antigens , injected during vaccination may be a significant starting factor of GN development in cats. Of no small importance is the fact that in human, for example, postinfectious GN develops weeks later after recovery from bacterial or viral infection, streptococcic or staphylococcic infection against the background of practically complete elimination of AG agent out of the organism.
Virus induced GN in cats, most probably develops under permanent pressing impact of various viral AG. Perhaps, in connection due to it exactly in cats CKD is diagnosed more often developed as a direct outcome of chronic course of GN. Non-immune infrequent and immune mediated inflammation of glomerule prevailing type of lesion are differentiated. GN of non-immune genesis secondary in most cases is a concomitant [coexistent] disease e. AG viral antigen, for example or its part initiates a cascade of responses which finally cause firstly necrosis of glomerular capillary net and then aseptic immune mediated inflammation.
As of today 2 types of process are well known - immune complex and antibody-mediated. The development mechanism of immune-complex GN is as follows. CIC circulating immune complex attach to endothelium of vessels in glomerule and phagocytize by Kupffer's cell or begin to eliminate through filter of glomerule damaging it.
Congregating in glomerule, CIC accumulate on the capillary vascular wall eventually causing microcirculation abnormality. The result of hypercoagulation is microthrombosis which lead to micronecrosis which finally causes reactive inflammation as a final stage of disease.
The source of antigenemia in GN with the antibody mechanism is a basic membrane of glomerule itself, previously damaged in some way including CIC or viral agents attack. But not important which exactly mechanism of pathologic development is responding, practically always there is only one outcome — chronic glomerulonephritis in cats develops.
Histologic pattern helps in diagnosing of in determining the etiology of the disease and in choosing of therapeutic decision for each particular patient.
Morphologically detected through an increased number of nucleus in the nodal part of glomerule and through swelling of fenestrated endothelium cells and mesangial matrix hipercelling and glomerule hypertrophy. Fig 1. Cat, female, 11 months. Fig 2. Cat, female, 9 years. Electron microscopy. Capillary lumen and mesangium areas. Luminal narrowing of capillary incomplete or absolute. Fig 5.
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Focal fibrinoid necrosis 2. Fig 6. In the majority of cases when changes in glomerule are evident, infiltration of cortical layer of kidney with agranular leukocytes lymphocytes, monocytes is observed. During the research it was discovered that agranulocytic infiltration of various severity appear in cortical layer of renal parenchyma in the majority of cats aged from 11 month to 22 years regardless of GN severity.
This fact indirectly corroborate the conjecture that the cause of GN development in cats are various chronic or latent viral infections which cause constant sensitization factor and, therefore, continuous filtration of circulating immune complex through glomerule for a lifelong period of an animals.
Fig 7. Cat, female, 7 years old. Fig 8. Cat, female, 11 years old. Focal periglomerular. Dilatation of urinary space. Cat, male, 14 years old. Cat, male, 15 years old. Polycystic renal disease. Pus collection in pathologic cavities 1. Can be either segmental when one capillary segment of glomerule is damaged or global. Global sclerosis results in total loss of glomerular function and is accompanied by fibrosis and atrophy of nephrons. It GS can arise on the basis of structural changes, described above or can be a primary.
In the absence of early diagnosis and proper complex therapy, the process of autoimmune inflammation of glomeruli rather quickly leads to sclerosis and subsequent involvement of all parts of nephron distension of tubules and atrophy of tubular epithelium are observed , and then whole cortical layer and medulla layer of kidney into pathologic process fig.
Fig Cat, female, 14 years old. Sclerosis of Bowman's capsule.
Collapse of capillary loop in glomerule. Female, 13 years old. Cystic dilatation of tubule, necrosis of tubular epithelium. Karyorrhexis in stroma nucleus debris of various size and shape in renal stroma. Hyaline cylinders in tubular lumen. Karyorrhexis nucleus debris of various size and shape in renal stroma.
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Dilatation of tubule. In cats, by hematogenic tract, bacteria can appear in renal parenchyma in great numbers only during pronounced immunodeficiency state, arising, for example, against extremely pathogenic and virulent viral infections viral leukemia, viral immunodeficiency, viral peritonitis in cats etc. However, impetuous colonization of renal parenchyma by bacteria in this case should be correctly identified as a pyo-granulomatosis, not pyelonephritis.
With polycystic kidney disease pus can fill pathologic cavities. But even in this case it is observed only in heavily broken animals. When GN onsets, glomeruli can be damaged to various degree, both all glomeruli and only the part of glomeruli. Focal type of lesion can be defined, when only part of glomeruli are damaged while others remain not affected and diffuse type of lesion, when all glomeruli are damaged.
At the final stages of development of pathologic process, apparent focal nephrosclerosis and karyorrhexis which is often precessed by pyknosis can be observed.
Clinicopathologic Principles for Veterinary Medicine
Clinical presentation of chronic glomerulonephritis in man has its typical pattern, and declares itself in the form of urinary syndrome, nephritic and nephrotic hypertension and congestive subcutaneous edema syndromes. However, chronic glomerulonephritis in cats, in most cases, and over a long period of time may manifests only with isolated urinary syndrome microhematuria and proteinuria , and possibly later can be attended by concomitant latent CRI abnormal [pathological] changes in blood examinations, however, clinical signs may be minor or may absent.
Just this fact is the basic issue with this pathology. Clinical signs usually they are nonspecific, asthenia, anorexia, vomiting, oliguria, health aggravation, skin and hair coat quality aggravation onset when pathosis has gone too far and considerable part of glomeruli were destroyed. Hydrosarca edema and hypertension, with the exception of severe cases of AKI, occur rarely.
Chronic glomerulonephritis is delayed-action bomb. Secondly, effect of any nephrotoxic agents such as aminoglycoside antibiotics, nonsteroidal anti-inflammatory drugs, NSAID non-steroidal anti-inflammatory drugs , cytostatic agent, heavy metal salts and stress s well, can lead to galloping renal insufficiency with fatal [lethal] termination. Laboratory diagnostics of biologic fluids helps not only to confirm indirectly tentative clinical diagnosis but also to detect associated pathology of other organs and systems.
In order to counteract infectious agents, the system has evolved to recognize molecular conformations foreign to the individual antigenic determi- nants and to promote their elimination. To accomplish this effectively, the system is ubiquitously distributed throughout body tissues and has as basic operational features: molecular recognition, amplification and memory, together with a range of effector pathways by which foreign material may be eliminated.
The last of these can be divided Ve tB oo ks. In addition, such a system requires precise regulation in order to avoid excessive and hence wasteful responses, and also potentially dangerous reactivity to self components.
These diverse activities are performed by a limited number of morphologically distinct cell types which are capable of migrating through the organs and tissues, performing their functions remote from their sites of origin and maturation. In this section, the chief features and interactions of these cells where considered germane to the main theme of this chapter will be reviewed briefly. Cells of the immune system The ability of the individual to recognize and respond to the intrusion of foreign macro- molecules resides in cells of the lymphoid series.
Lymphoid cells are distributed throughout the body both in circulating fluids and in solid tissues. In the latter, they occur either diffusely or in aggregates of varying degrees of organization. In strategic regions of the body, they collectively form discrete encapsulated lymphoid organs such as the spleen and lymph nodes. The central cell of lymphoid tissues is the immunocompetent lymphocyte.
These cells have receptor molecules on their cytoplasmic antigenic stimulation resting lymphocyte effector cells B or T blast transformation proliferation Fig. Resting lymphocytes following contact with an appropriate antigen undergo blast transformation followed by proliferation and further differentiation. Lymphocytes are activated by contact with appropriate antigenic determinants and then undergo transformation, proliferation and further differentiation Fig. Ultimately, one or more effector pathways are initiated and the antigen concerned may then be elimin- ated.
Activated cells secrete a variety of bio- logically active effector molecules which are responsible both for cellular regulation and effector functions. In addition, a proportion of the expanded cell population remains dor- mant as memory cells and accounts for the augmented secondary response on re- exposure to the same antigen. Lymphocytes are divided into B and T cell classes on the basis of ontogeny and function.
Functionally, B lymphocytes are responsible for humoral, and T lymphocytes for cell-mediated immune responses. These cells also differ in their distribution within lymphoid tissues and in their expression of cell surface molecules markers. Thus the immune system can be regarded as a system composed of dual but interacting compart- ments.
The B lymphocyte Cells of this lineage are the progenitors of anti- body-secreting plasma cells and in mammals develop initially from stem cells situated in the bone marrow by a process of antigen-indepen- dent maturation. Subsequently, after migration to peripheral lymphoid tissues, they undergo further differentiation induced by antigen contact and mature to plasma cells. Depending on the nature of antigen con- cerned, B cell activation may require the cooperation of a subpopulation of T cells T helper cells.
Generally, small asymmetric molecules such as polypeptides will not stimu- late B cells directly, and require T cell cooper- ation, whilst many polysaccharides are capable of causing a direct but limited B cell response.
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