The kidney fulfills three major functions: (1) elimination of waste products, (2) homeostasis of water and acid/base balance, and (3) as an endocrine organ the production of erythropoietin, renin/angiotensin, and conversion of vitamin D to its most active form, 1,25-dihydroxycholecalciferol to aid in intestinal calcium resorption. Additional functions are activation/deactivation of polypeptide hormones such as insulin and glucagon, and the local production of prostaglandins.
The kidney is a filtration-resorption organ and relatively simple in its mode of operation in regulating the salt and water balance and excretion of nitrogen metabolites. The nephron is the basic functional unit of the kidney. The nephron consists of a single glomerulotubular unit. There are 1–2 million nephrons per human kidney giving it a large functional reserve; a loss of 75% of nephrons still maintains renal function.
The kidneys are richly supplied by blood vessels. In healthy human individuals, about a quarter of the cardiac output is delivered to the kidneys. Approximately 180 liters per 24 hours are filtered through the human glomerular capillaries.
In terms of primary renal pathologic processes, there are developmental abnormalities, glomerular diseases, tubular diseases, pelvic diseases, vascular diseases, and neoplasms.
I. Kidney
1. Abnormalities
These include renal aplasia, hypoplasia, dysplasia, fused kidneys (horseshoe kidneys), persistent lobulation, and renal cysts.
Figure 8.1. Horse. Kidney. Polycystic Kidney. Thin-walled clear fluid distensions are visible in the cortex. Multiple cysts are usually primary developmental abnormalities. Individual cysts may develop secondarily to inflammation and fibrosis.
Figure 8.2. Horse. Kidneys. Bilateral Hypoplasia/Dysplasia. Various segments of the final kidney architecture arise from different embryologic components. Dysplasia has been defined as abnormal renal structural organization and differentiation. Dysplasia can be unilateral or bilateral. Bilateral in foals after EPM treatment of pregnant mare with trimetoprim sulfa supplemented with folic acid.
Figure 8.3. Horse. Kidney. Horseshoe Kidney. It is the result of fusion of the cranial or caudal poles of the two kidneys during organ development. Histology and function are normal.
2. Circulatory disturbances
a. Hemorrhage
Hemorrhage results from trauma, bleeding disorders, or vascular insults. Petechiations are reflections of sepsis.
b. Infarcts
Renal infarcts occur from vascular occlusions by thromboemboli showered from different sources, usually the heart. Infarcts are hemorrhagic when acute and white when chronic. They are typically wedge shaped. The size depends on the caliber of the occluded vessel.
Figure 8.4. Horse. Kidney. Chronic Infarct. A yellowish triangular focus in the cortex is discretely delineated from the normal cortical parenchyma.
3. Metabolic disturbances
Figure 8.5. Horse. Kidney. Lipidosis. The kidney is yellow and soft on touch. It belonged to a pregnant mare with severe obesity. Differential diagnoses for pallor are nephrosis, anemia, fibrosis, and autolysis.
4. Inflammatory and infectious diseases
Inflammatory disease may be acute and chronic. Inflammation in the kidney may involve glomeruli, the tubulointerstitial apparatus, and the pelvis. Overlapping forms are common. Glomerulitis may lead to glomerulonephritis and pyelitis to pyelonephritis. Clinical presentation of primary glomerular disease is proteinuria; primary tubular disease clinically results in uremia, polyuria, electrolyte loss, acid/base imbalance, and ultimately renal failure.
If infectious agents are involved, these can either reach the kidneys hematogenously or ascending from the lower urinary tract (urogenously). Infectious agents in horses usually are bacteria. Rarely are viruses, parasites, and fungi involved.
Figure 8.6. Horse. Kidney. Chronic Glomerulonephritis, Fibrosis, and Renal Calculi. The kidney is pale green and firm. Stripping the capsule will lead to tearing of the cortical surface. The cortex is poorly outlined. Small renal calculi are lodged in the pelvis. With no compensation possible, renal failure is the clinical outcome of these end-stage morphologic changes if both kidneys are involved.
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