Acquired cystic kidney disease is a form of kidney disease that develops in later stages of chronic kidney disease and most commonly after a patient has started to undergo dialysis to clean the blood.
Acquired cystic kidney disease differs from other forms of kidney diseases with cyst development in that it is fairly asymptomatic. The patient rarely feels much from the presence of the cysts in their kidneys. The kidney tends to remain the same size rather than expand due to the fluid filled sacs. Thus unlike polycystic kidney disease where the gradually expanding kidneys can be uncomfortable for the patient, an individual with the acquired cystic kidney disease can be oblivious to the structures developing inside them.
The presence of the cysts may become apparent should a cyst burst. This can cause the patient to feel pain or possibly develop a fever. Further investigation would then potentially reveal the cause. Signs of the disease can also include blood in the urine, a lump in the stomach, reduced appetite, pain at the side of the body, anemia and weight loss.
Another potential complication is that a cyst may become cancerous and cause renal cell carcinoma. This occurs in about 7% of cases, and the cancer is located in the tubules of the kidney. These are the structures that help to filter the blood from the kidney and create the urine that we excrete from our bodies.
The longer a person has dialysis, the higher the risk is of them developing renal cell cancer as a result of acquired cystic kidney disease as this disease becomes more likely with the length of time that a person experiences end stage renal disease.
The initial kidney failure, also known as end stage renal disease, that triggers the development of acquired cystic kidney disease can be caused by a number of different triggers such as diabetes, lupus, heart problems and urinary tract conditions. These diseases can result in permanent damage to the kidneys. Genetic diseases can also be implicated in the deterioration of the kidneys; however, acquired kidney disease is not by itself a hereditary disease.
Many researchers hypothesize that nephron loss of any etiology results in compensatory tubular cell hyperplasia in the intact nephrons. This response usually starts by activation of proto-oncogenes and release of various growth factors, which in turn accumulate in patients with chronic kidney insufficiency. Over a prolonged period of time, these factors then lead to tubular hyperplasia and subsequent cyst formation.
Regardless of such hypotheses, the causes of the cysts in acquired cystic kidney disease are not yet fully understood. The cysts only develop in the kidneys and nowhere else in the patient so are considered to occur as a result of activity in this area but this has not been proved. It has been suggested that they are a result of the build-up of waste products that the kidneys, with male hormones also playing a role. The lack of knowledge in the field means that the disease cannot currently be cured.