See below for my answer to each one of your questions. This requires two posts, because its a long one!:
in ESRD, there is impaired ammonia excretion, reduced tubular bicarbonate reabsorption and insufficient renal bicarbonate production in relation to the amount of acids synthesized by the body and ingested with food. This in turn results in much more acid being present in the body compared to the basic bicarbonate, explaining the metabolic acidosis.
It can be caused by reduced renal excretion, excessive intake or leakage of potassium from the intracellular space
Hypocalcemia in chronic renal failure is due to two primary causes - increased serum phosphorus and decreased renal production of 1,25 (OH)2 vitamin D. The former causes hypocalcemia by complexing with serum calcium and depositing it into bone and other tissues.
Increased BUN and serum creatinine
Urea nitrogen is a normal waste product in your blood that comes from the breakdown of protein from the foods you eat and from your body metabolism. It is normally removed from your blood by your kidneys, but when kidney function slows down, the BUN level rises.
Creatinine is a waste product in your blood that comes from muscle activity. It is normally removed from your blood by your kidneys, but when kidney function slows down, the creatinine level rises.
The peri-tubular cells of the kidney are responsible for secreting erythropoietin a condition in which you lack enough healthy red blood cells to carry adequate oxygen to your body's tissues, specifically when you have a decrease in RBC mass. So, without enough EPO, you get an anemia! Specifically, Anemia of Chronic Renal disease
Patients with ESRD traditionally have low platelet counts. Low platelets would lead to impaired clotting (something called thrombocytopenia). Platelet clotting is also dependent on key factors, including ADP and serotonin. These molecules induce platelet aggregation and degranulation, allowing for a primary hemostatic plug to be formed. Under normal conditions, ADP and serotonin are secreted to attract more platelets. In renal failure patients, their platelet granules have decreased levels of ADP and serotonin.
Platelet dysfunction in renal failure can also be attributable to high levels of small molecules known as uremic toxins, hence the term “uremic thrombocytopathy.” Although a variety of moieties contribute to platelet dysfunction or abnormal interactions between platelets and the vascular wall, urea remains a potential factor.
Edema means swelling or fluid retention. The edema associated with kidney disease usually occurs in your legs and around your eyes. Kidney damage. Damage to the tiny, filtering blood vessels in your kidneys can result in nephrotic syndrome. In nephrotic syndrome, declining levels of protein (albumin) in your blood can lead to fluid accumulation and edema. Based on osmolarity fluid principles, where there is more protein, water will flow. Hence more protein deposition in the tissue will induce water to flow into tissues causing edema.