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Nephropathy is a broad medical term used to denote disease or damage of the kidney, which can eventually result in kidney failure. The primary and most obvious functions of the kidney are to excrete any waste products and to regulate the water and acid-base balance of the body – therefore loss of kidney function is a potentially fatal condition.
Nephropathy is considered a progressive illness; in other words, as kidneys become less and less effective over time (with the progression of the disease), the condition of the patient gets worse if left untreated. This is the reason why it is pivotal to receive adequate diagnosis and treatment as early as possible.
Diabetic nephropathy is considered a major microvascular complication of diabetes mellitus that affects approximately one-third of all diabetic patients. It usually accompanies albuminuria with glomerular hyperfiltration and renal hypertrophy in the early stage, often showing a deteriorating course that can lead to end-stage renal failure.
Histopathologically, diabetic nephropathy is characterized by glomerulosclerosis with thickening of the glomerular basement membrane, abnormalities of podocytes (terminally differentiated cells located in the Bowman’s capsule of the kidney) and extracellular matrix accumulation in the glomerular mesangial area.
Proper management of hyperglycemia, hypertension and serum lipid levels is pivotal in the prevention of the onset and progression of nephropathy in diabetic patients. Nevertheless, no available treatment has been able to halt the progression to end-stage renal failure, thus new therapeutic modalities to manage diabetic nephropathy are desperately needed.
The diagnostic hallmark of the disease is the deposition of IgA antibodies in the glomeruli, alone or together with IgM or IgG antibodies. Activation of innate immune response and complement, as well as the formation of immune complexes, play a significant role in clinical presentation and severity of the IgA nephropathy.Since its initial description in 1968, IgA nephropathy remains the most common form of primary glomerulonephritis that can lead to chronic kidney disease. This condition is very commonly observed in Southern Europe and Asia, whereas in Northern climates of the Western World the incidence is approximately 5-10% of all biopsies for glomerulonephritis.
As there is no pathognomonic clinical presentation (although young males with macroscopic hematuria following an upper respiratory tract infection are highly suspicious for the disease), the diagnosis requires renal biopsy. Presently available treatment options are directed towards inflammatory and immune events that can result in renal scarring.
Analgesic nephropathy is a chronic renal disease caused by excessive and prolonged consumption of analgesic mixtures that contain phenacetin or two other analgesics, such as salicylic acid-paracetamol, salicylic acid-pyrazolones, paracetamol-pyrazolones or two pyrazolones combined with potentially addictive substances such as codeine or caffeine.
Renal papillary necrosis (i.e. damage to the inner medulla caused by capillary sclerosis) represents the characteristic feature of analgesic nephropathy, and most often arises as a result of a long term use of phenacetin. Renal complications that can ensue are acute or chronic pyelonephritis, calcification of necrotic papillae, urolithiasis and uroepithelial tumors.
Acute uric acid nephropathy stems from the intratubular deposition of uric acid crystals when a high serum uric acid concentration is present. This condition usually occurs during induction chemotherapy for malignancies with high cell turnover. Recommended treatment options for this condition are alkalization of the urine and a drug known as rasburicase (a recombinant urate oxidase).