What is Diabetic Nephropathy?Diabetic nephropathy (''nephropatia diabetica''), also known as Kimmelstiel-Wilson syndrome and intercapillary glomerulonephritis, is a progressive kidney disease caused by angiopathy of capillaries in the kidney glomeruli. Diabetes is a disease that is characterized by the inability of the body to regulate the blood sugar levels, mainly due to either lack of or decreased sensitivity to the insulin hormone. It is a disease which affects the entire body and if the blood sugar levels stands above normal, for a considerable period of time, then the complications starts.  Diabetic neuropathy is one such condition where the nerves are affected due to persistent excess glucose in the blood. The most common and the most widely known complication of diabetes is peripheral neuropathy.
So when the foot is cut or any injury occurs to the leg or foot, the damage to the nerves renders the part insensitive to pain. Diabetic autonomic neuropathy affects several organs like the stomach, blood vessels, urinary organs and the sex organs.When the stomach is involved there is often flatulence and bloating, constipation or diarrhea and other symptoms normally linked to acidity like heart burn, nausea etc. If the autonomic neuropathy invilves the blood vessels that would cause dizziness and fainting spells. Proper foot care and management of minor foot injuries, like scrapes, cuts or blisters, are the best way to prevent an ulcer from developing. Ensuring your shoes properly fit and are not squeezing tightly around your feet is also key in prevention. The hallmark of CRPS is pain and mobility problems out of proportion to those expected from the initial injury. Complex Regional Pain Syndrome is the new term for what we used to call RSD or causalgia.  Symptoms can develop into CRPS from a major nerve injury (CRPS Type II) or from minimal or no trauma (CRPS Type I). The first stage typically lasts about 3 months and starts with severe, burning localized pain, hyperesthesia, localized edema, stiffness and vasospasm (warm, red and dry at first, then changes to cyanotic, cold and sweaty).
CRPS is associated with a variety of skin disorders including rashes, ulcers and pustules.  Although extremely rare, some patients have required amputation of an extremity due to life-threatening recurring infections of the skin. Evaporative skin testing with loss of temperature discrimination and development of allodynia upon evaporation is a useful screening tool.
Electrodiagnostic testing to exclude nerve entrapment as well as Neurodiagnostic imaging may be necessary to exclude a neuraxial pathology, such as a bulging disc. Early diagnosis in the first six months to maximal two years is the key to successful treatment. Management options include sympathetic blocks utilizing regional anesthetic techniques and radiofrequency thermoneurolysis or neuromodulation with spinal cord stimulation or peripheral nerve stimulation.  Radiofrequency neurolysis is an extension of a continuous regional sympathetic block or neurolytic block providing long-term relief with added safety. Consideration of sympathetic blocks is to facilitate management of CRPS with analgesia commensurate with a program of functional restoration and sympatholysis to provide unequivocal evidence of sympathetically maintained pain.
Radiofrequency has been described for lesioning of the cervical sympathetic chain, thoracic sympathetic chain, and lumbar sympathetic chain, in cases of CRPS I and II, as well as for neuropathic pain. The insulin hormone is mainly produced by the pancreas and the production is regulated by a complex mechanism.
The diabetic neuropathy is not focused on a single system, rather there are a wide variety of functions that are hampered.
In peripheral neuropathy, the part of the body that is most affected are the legs and feet.
The autonomic neuropathy of the bladder is mainly linked with frequency of urination or leaking of urine involuntarily.


Carpal tunnel syndrome is another complication of diabetic neuropathy in which the median nerve gets trapped in the carpal tunnel which is situated near the wrist.This results again in pain and numbness. These painful sores often develop at the bottom of the feet and typically take weeks to several months to heal, explains Greensboro podiatrist, Dr.
The balls and sides of the feet, or the bottom of the big toe, are typically where the ulcers appear. Daily foot inspections, cleansing your feet with soap and water, as well as using topical moisturizers, are the best way to maintain healthy skin and prevent the breakdown of the skin of your feet. Many people have found that custom diabetic shoes and thick absorbent socks have helped them avoid ulcer formation. Abnormal sympathetic (vasomotor changes) activity may be associated with skin that is either warm or cold to touch. Processes in the spinal cord as well as supraspinal changes are responsible for spontaneous spread in CRPS to other extremities.
Surgical sympathectomy procedures (removal of a part of the chain of sympathetic ganglia on the side of the spine) have limited application for the treatment of RSD. Once it is established that sympatholysis is effective in relieving not only the burning dysesthesia but also allodynia or hyperalgesia, it is important to repeat the procedure to determine whether an increasing duration of effect can be expected in any particular patient. Neuropathy involves damage to bones, so peripheral neuropathy is associated with loss of sensations in the affected part. This could lead to the development of diabetic ulcer, which is yet another complication of diabetes.
The patient may perceive sensations of warmth or coolness in the affected limb without even touching it (vasomotor changes). If this is the case, these individual blocks may be all that are necessary to enable a patient to regain function.
The disease is progressive and may cause death two or three years after the initial lesions, and is more frequent in men. The symptoms that helps in identifying the development of peripheral neuropathy would be numbness, tingling, burning sensation in the legs and pain. The skin may show increased sweating (sudomotor changes) or increased chilling of the skin with goose flesh (pilomotor changes). When sympatholysis completely relieves the symptoms and facilitates exercise therapy but is limited to its duration of effect, it is appropriate to consider a prolonged block using radiofrequency neurolysis. Diabetic nephropathy is the most common cause of chronic kidney failure and end-stage kidney disease in the United States. Constriction of the blood vessels or deposits forming on these blood vessels all lead to micro vascular injury.
Changes in skin color can range from a white mottled appearance to a red or blue appearance. Changes in skin color (and pain) can be triggered by changes in the room temperature, especially cold environments. There may be diffuse tenderness or point-tender spots in the muscles of the affected region due to small muscle spasms called muscle trigger points (myofascial pain syndrome).
Further, once nephropathy develops, the greatest rate of progression is seen in patients with poor control of their blood pressure.


There may be spontaneous sharp jabs of pain in the affected region that seem to come from nowhere (paroxysmal dysesthesias and lancinating pains).
Also people with high cholesterol level in their blood have much more risk than others.The earliest detectable change in the course of diabetic nephropathy is a thickening in the glomerulus. At this stage, the kidney may start allowing more serum albumin (plasma protein) than normal in the urine (albuminuria), and this can be detected by sensitive medical tests for albumin. As diabetic nephropathy progresses, increasing numbers of glomeruli are destroyed by nodular glomerulosclerosis. Now the amounts of albumin being excreted in the urine increases, and may be detected by ordinary urinalysis techniques.
At this stage, a kidney biopsy clearly shows diabetic nephropathy.Diabetic nephropathy continues to get gradually worse. Complications of chronic kidney failure are more likely to occur earlier, and progress more rapidly, when it is caused by diabetes than other causes. The main treatment, once proteinuria is established, is ACE inhibitor drugs, which usually reduces proteinuria levels and slows the progression of diabetic nephropathy. Several effects of the ACEIs that may contribute to renal protection have been related to the association of rise in Kinins which is also responsible for some of the side effects associated with ACEIs therapy such as dry cough. The renal protection effect is related to the antihypertensive effects in normal and hypertensive patients, renal vasodilatation resulting in increased renal blood flow and dilatation of the efferent arterioles. Many studies have shown that related drugs, angiotensin receptor blockers (ARBs), have a similar benefit. However, combination therapy, according to the ONTARGET study, is known to worsen major renal outcomes, such as increasing serum creatinine and causing a greater decline in estimated glomerular filtration rate (eGFR).Blood-glucose levels should be closely monitored and controlled. As kidney failure progresses, less insulin is excreted, so smaller doses may be needed to control glucose levels.Diet may be modified to help control blood-sugar levels.
Modification of protein intake can effect hemodynamic and nonhemodynamic injury.High blood pressure should be aggressively treated with antihypertensive medications, in order to reduce the risks of kidney, eye, and blood vessel damage in the body. Urinary tract and other infections are common and can be treated with appropriate antibiotics.Dialysis may be necessary once end-stage renal disease develops. These include, but are not limited to, bardoxolone methyl, olmesartan medoxomil, sulodexide, and avosentan This article is licensed under the Creative Commons Attribution-ShareAlike License. There is an increase in blood pressure (hypertension) and fluid retention in the body plus a reduced plasma oncotic pressure causes oedema. Other complications may be arteriosclerosis of the renal artery and proteinuria.Throughout its early course, diabetic nephropathy has no symptoms.
Most often, the diagnosis is suspected when a routine urinalysis of a person with diabetes shows too much protein in the urine (proteinuria). The urinalysis may also show glucose in the urine, especially if blood glucose is poorly controlled. Serum creatinine and BUN may increase as kidney damage progresses.A kidney biopsy confirms the diagnosis, although it is not always necessary if the case is straightforward, with a documented progression of proteinuria over time and presence of diabetic retinopathy on examination of the retina of the eyes.



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