Chronic renal failure history and symptoms: Difference between revisions
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** Later this progresses to [[tertiary hyperparathyroidism]], with [[hypercalcaemia]], [[renal osteodystrophy]] and vascular calcification | ** Later this progresses to [[tertiary hyperparathyroidism]], with [[hypercalcaemia]], [[renal osteodystrophy]] and vascular calcification | ||
* [[Metabolic acidosis]], due to decreased generation of [[bicarbonate]] by the kidney, leads to uncomfortable breathing and further worsening of bone health. | * [[Metabolic acidosis]], due to decreased generation of [[bicarbonate]] by the kidney, leads to uncomfortable breathing and further worsening of bone health. | ||
CRF patients suffer from accelerated [[atherosclerosis]] and have higher incidence of [[cardiovascular disease]], with a poorer prognosis. | |||
In many CRF patients, previous renal disease or other underlying diseases are already known. A small number presents with CRF of unknown cause. In these patients, a cause is occasionally identified retrospectively. | |||
It is important to differentiate CRF from [[acute renal failure]] (ARF) because ARF can be reversible. Abdominal [[medical ultrasonography|ultrasound]] is commonly performed, in which the size of the [[kidney]]s are measured. Kidneys in CRF are usually smaller (< 9 cm) than normal kidneys with notable exceptions such as in [[diabetic nephropathy]] and [[polycystic kidney disease]]. Another diagnostic clue that helps differentiate CRF and ARF is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). If these levels are unavailable (because the patient has been well and has had no blood tests) it is occasionally necessary to treat a patient briefly as having ARF until it has been established that the renal impairment is irreversible. | |||
Numerous uremic toxins (see link) are accumulating in chronic renal failure patients treated with standard dialysis. These toxins show various cytotoxic activities in the serum, have different molecular weights and some of them are bound to other proteins, primarily to albumin. Such toxic protein bound substances are receiving the attention of scientists who are interested in improving the standard chronic dialysis procedures used today. | |||
==[[References]]== | ==[[References]]== | ||
Revision as of 15:50, 17 July 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]
History and symptoms
Initially it is without specific symptoms and can only be detected as an increase in serum creatinine. As the kidney function decreases:
- Blood pressure is increased due to fluid overload and production of vasoactive hormones leading to hypertension andcongestive heart failure
- Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis andencephalopathy)
- Potassium accumulates in the blood (known as hyperkalemia with symptoms ranging from malaise to fatal cardiac arrhythmias)
- Erythropoietin synthesis is decreased (leading to anemia causing fatigue)
- Fluid volume overload - symptoms may range from mild edema to life-threatening pulmonary edema
- Hyperphosphatemia - due to reduced phosphate excretion, associated with hypocalcemia (due to vitamin D3 deficiency).
- Later this progresses to tertiary hyperparathyroidism, with hypercalcaemia, renal osteodystrophy and vascular calcification
- Metabolic acidosis, due to decreased generation of bicarbonate by the kidney, leads to uncomfortable breathing and further worsening of bone health.
CRF patients suffer from accelerated atherosclerosis and have higher incidence of cardiovascular disease, with a poorer prognosis.
In many CRF patients, previous renal disease or other underlying diseases are already known. A small number presents with CRF of unknown cause. In these patients, a cause is occasionally identified retrospectively.
It is important to differentiate CRF from acute renal failure (ARF) because ARF can be reversible. Abdominal ultrasound is commonly performed, in which the size of the kidneys are measured. Kidneys in CRF are usually smaller (< 9 cm) than normal kidneys with notable exceptions such as in diabetic nephropathy and polycystic kidney disease. Another diagnostic clue that helps differentiate CRF and ARF is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). If these levels are unavailable (because the patient has been well and has had no blood tests) it is occasionally necessary to treat a patient briefly as having ARF until it has been established that the renal impairment is irreversible.
Numerous uremic toxins (see link) are accumulating in chronic renal failure patients treated with standard dialysis. These toxins show various cytotoxic activities in the serum, have different molecular weights and some of them are bound to other proteins, primarily to albumin. Such toxic protein bound substances are receiving the attention of scientists who are interested in improving the standard chronic dialysis procedures used today.