Hepatic Lipidosis Most common form of severe liver disease in cats. Most often seen in obese cats suddenly subjected to dietary deprivation. May also be associated with diabetes mellitus, drug injury and toxicity. Thedisease seems to result from the sudden mobilisation of the bodies fat stores which quickly overwhelms the liver's ability to process the raw fat into useful nutrients. The fat accumulates in the liver rapidly and causes acute liver failure. The end result is a swollen, greasy liver which is fragile and yellow to see. The cats present with complete lack of appetite and many signs of acute liver failure. Treatment is based on the provision of a highly nutritious diet to provide the energy required to run the body, stop the ongoing mobilisation of the fat stores, and drive the liver to decrease the fatty accumulation in the liver. Treatment is difficult and a long process.
Atrophied kidneys is an abnormal kidney condition and can be caused by many illness conditions. When there is renal atrophy, the renal glomeruli and renal tubules will be damaged and the kidney functions will be people with strophic left kidney caused by kidney failure, they will have a series of symptoms and discomforts including nausea, vomiting, fatigue, anemia, swelling in eyes and legs, itching skin and severe back pain. Blood pressure will increase as renal atrophy becomes worse and patients will also lose weight. In addition, some patients can even have hematuria. Patients will begin to have renal dysfunction and renal failure. Therefore it is very crucial to control and improve the atrophic kidneys.
Acute phosphate nephropathy with intratubular calcium phosphate deposition that somewhat resembles the pathology of our patients is caused by oral sodium phosphates used for bowel preparation before colonoscopy [ 24 ]. Protein powder contains little inorganic phosphate with three daily supplement servings providing < g [ 25 ]. Creatine is sold mainly in the form of a monohydrate also with little phosphorus. Daily 2–3 L milk consumption will add – g to a normal dietary phosphorus intake of – g [ 25 ]. This is well below the 11 g oral intake used in bowel preparations [ 24 ]. In addition, the negative von Kossa stains indicates that the mainly amorphous tubular concretions found in the kidneys of our patients were acutely precipitated and had not complexed into crystalline hydroxyapatite with prominently stained phosphates that are seen in hyperphosphatemic nephropathy as well as other forms of neprocalcinosis [ 26 ].