Treatment principles of Purpura Nephritis

HSPN should be treated with different schedules according to patients’ ages, clinical presentations, and the levels of kidney damage.
Positively control immune inflammatory response; restrain glomerular mesentery proliferative lesion; prevent and delay the forming of chronic renal fibrosis lesion.

Treatment
Pain killers may be needed for the abdominal and joint pains. It is uncertain as to whether HSP needs treatment beyond controlling the symptoms. Most patients do not receive therapy because of the high spontaneous recovery rate. Steroids are generally avoided.However, if they are given early in the disease episode, the duration of symptoms may be shortened, and abdominal pain can improve significantly. Moreover, the chance of severe kidney problems may be reduced.However, some evidence suggests that steroids do not decrease the likelihood of developing long-term kidney disease.

Evidence of worsening kidney damage would normally prompt a kidney biopsy. Treatment may be indicated on the basis of the appearance of the biopsy sample; various treatments may be used, ranging from oral steroids to a combination of intravenous methylprednisolone (steroid), cyclophosphamide and dipyridamole followed by prednisone. Other regimens include steroids/azathioprine, and steroids/cyclophosphamide (with or without heparin and warfarin). Intravenous immunoglobulin (IVIG) is occasionally usually.

Plasma exchange
PN, whose clinical presentations are progressive nephritis and a large number of crescents (>50%) formation in kidney biopsy, has a high risk of developing terminal renal failure. For these severe cases, they should be take positive measures, such as plasma exchange. It’s indicate in clinical practice that using hormone and cytotoxic drugs, using together with plasma exchange,or using plasma exchange alone, can reduce renal damage and delay the development of renal failure.

If you still have any follow-up questions, you are welcomed to leave us a message or you can send us an email to doctornickzhnag@hotmail.com.

Diet with Purpura Nephritis

Purpura is purple-colored spots and patches that occur on the skin, organs, and in mucus membranes, including the lining of the mouth.

What is purpura nephritis?
The disease, just as its name denotes, is caused by HSP. How? The kidneys get involved because of immune complexes just like any other kidney disease. What are the immune complexes in this disease? They are IgA and C3. Those immune complexes deposit in kidneys through the blood flow. Renal blood capillary and intrinsic cells are infected accordingly.

How should patients with Purpura Nephritis eat?
1.Intake of salt
If patients with Purpura Nephritis do not have symptoms of edema and high blood pressure, they need not limit intake of salt. Under this condition, they can take 10 gram of salt each day as normal people. Patients with edema and high blood pressure should limit intake of salt. If patients do not limit intake of salt, retention of sodium and water will aggravate and edema is difficult to be removed, which will lead to a rise in blood pressure. Generally speaking, patients should take 2-3 gram of salt. Patients with oliguria and increased blood potassium should limit intake of sylvite.
2. Intake of water
If patients with Purpura Nephritis do not have symptoms of oliguria and edema, they need not control the intake of water. Patients with edema should control intake of water mainly according to urine volume and the degree of edema. Generally speaking, if the symptom of edema is obvious, patients should limit the intake of water within 500-800 ml/day except eating food.
3. Patients with Purpura Nephritis should have a good rest when they receive treatment. Patients with serious conditions can not take a bath themselves for a long time, which can avoid cold and overfatigue. Patients can not wash the clothes and exercise for a long time. Patients should avoid riding a bicycle. They should set up the confidence of conquering disease.

If you still want to know more about diet with Purpura Nephritis or its best treatment, you are welcomed to send us an email to doctornickzhang@hotmail.com, or leave us a message.

Henoch-Schönlein Purpura Nephritis Causes and Its Relationship with IgA

Henoch-Schönlein purpura nephritis is a rare kidney disease leading to chronic kidney disease. Although retrospective studies suggest beneficial effects of some therapies, prospective randomized clinical trials proving treatment efficacy are still lacking. In view of this, we should find out its causes and then prevent them.

Henoch-Schonlein purpura is a type of vasculitis and inflammatory response within the blood vessel that has symptoms of purple spots on the skin, joint pain, gastrointestinal symptoms, and glomerulonephritis. It is usually seen in children (more commonly boys than in girls), but people of any age may be affected. Many have had an upper respiratory illness in the previous weeks. However, the pathogenesis of HSP remains unknown.

It is generally considered to be an immune complex-mediated disease characterized by the presence of polymeric IgA1containing immune complexes predominantly in dermal, gastrointestinal, and glomerular capillaries. The pathognomonic granular IgA and C3 deposits in the mesangium are indistinguishable from those seen in IgA nephropathy. Similar immunohistologic findings have also been observed in the kidneys of patients with liver cirrhosis, dermatitis herpetiformis, celiac disease, and chronic inflammatory disease of the lung.

The relationship between IgA nephropathy and HSP remains obscure, since the pathogenesis of both are still enigmatic despite the considerable information presented. However, a good deal of evidence suggests that the two disorders are pathogenetically linked. Many (but not all) patients with both disorders have increased serum IgA levels and IgA-containing CIC. Other observations in favor of a hypothesis of commonality include the indistinguishable nature of the renal histopathologic lesion, the presence of clinically silent but histologically detectable IgA deposits in dermal and gastrointestinal tissue in patients with Berger's disease, and the occasional report of HSP occurring in patients with prior long-term IgA nephropathy. Finally, one of two identical twin brothers simultaneously infected by proven adenovirus developed severe HSP nephritis progressing to chronic renal insufficiency, while the other developed Berger's disease with recurrent asymptomatic hematuria.