Nephritis is a serious disease - in this case, home treatment will not help. Nephritis - whether it's glomerulonephritis, interstitial nephritis, or pyelonephritis - requires consultation with your doctor. What are the causes and symptoms of nephritis? What is the treatment? What diet is recommended?

Nephritisis a disease in which the kidneys are inflamed. There are glomerulonephritis, interstitial nephritis and pyelonephritis. Regardless of the type of nephritis, specializedtreatmentis necessary - thishomewill not help, and may even exacerbatesymptomssickness. The consequence may be dangerouscomplications .

Glomerulonephritis

1. Acute glomerulonephritis

Acute streptococcal glomerulonephritis

Reasons

Acute post-streptococcal glomerulonephritis is an immunologically determined form of glomerulopathy [or glomerular disease] that occurs after a history of infection with group A β-hemolytic streptococci of the respiratory tract or skin. The recovery period after a respiratory tract infection is interrupted after about 2-3 weeks by the appearance of kidney symptoms, which are the result of the accumulation of immune complexes in the renal glomeruli and the activation of complement [or immune protein].

Symptoms

About 2 weeks after the end of an acute pharyngeal or skin infection, symptoms of general weakness appear, accompanied by microhematuria [haematuria] and proteinuria. It occurs less frequently:

  • hypertension
  • puffiness
  • pains in the lumbar region
  • headaches
  • sleepiness
  • seizures as a result of brain edema

There may also be a hypertensive crisis with symptoms of left ventricular failure such as pulmonary edema and shortness of breath. It is worth knowing that in half of the patients the course may be asymptomatic.

Diagnostics and tests

The general examination of the urine shows erythrocyturia, proteinuria and red cell rolleruria, and blood counts show an increase in creatinine and urea concentrations,increase in antistreptolysin and anti-DNAase B titers as well as decreased complement concentration.

For the diagnosis of acute post-streptococcal glomerulonephritis, the most important is a history of streptococcal infection, presence of streptococci in swabs from the throat or skin, an increase in ASO (anti-streptolysin) titer and a decrease in complement concentration.

The differential diagnosis includes Berger's disease and rapidly progressing glomerulonephritis.

Treatment

Treatment is based on the use of antibiotics active against established streptococci, as well as limiting fluid intake and administering loop diuretics in the presence of edema. In patients with arterial hypertension, it is recommended to administer antihypertensive drugs, such as calcium channel blockers, convertase inhibitors, sartans or beta-blockers. In addition, patients are recommended to limit the supply of proteins.

Prognosis

Complete recovery is observed in about 90% of children and 50 percent. adults. Death may be the result of body fluid overload and a hypertensive crisis. It is worth remembering that the persistence of trace hematuria or proteinuria for a period of several months may be the first symptom of the chronicisation of the disease process, which may lead to the development of chronic uremia after years.

Holding Urine Harms Your Kidneys! [TOWIDEO]

Acute post-infectious glomerulopathy

Is caused by sepsis caused by bacteria other than streptococci (eg Meningococcus, Pneumococcus, Salmonella), viruses (eg HBV, HIV) or parasites. The symptoms of patients are usually milder than those of post-streptococcal glomerulopathy. It is worth remembering that the disease is usually completely healed once the infection is under control.

Acute glomerulopathies in the course of systemic diseases

Diseases causing this type of glomerulonephritis include systemic lupus, Good-pasture syndrome, Schӧnlein-Henoch disease, and certain forms of vasculitis in the course of Wegener's or Churg-Strauss syndrome.

a) LUPUS KIDNEY COMPLICATIONS

Causes: Nucleosomes have the greatest share in the development of renal complications in the course of systemic lupus. Joining the cationic part of the nucleosome with the anionic components of the capillaries causes deposits of nucleosomes and anti-nucleosomal antibodies to form in the renal glomeruli.

Symptoms: In addition to general lupus symptoms such as:

  • skin eruptions
  • hair loss
  • painsjoints
  • serous membrane inflammation

there are renal symptoms that depend on the type and extent of glomerular changes. In the presence of minimal changes in the renal glomeruli, slight proteinuria, hematuria, and red cell rolleruria are present. However, in patients with membranous or membranous hyperplastic changes - nephrotic syndrome occurs.

Diagnostics, tests: They are determined on the basis of the characteristic clinical picture as well as the presence of anti-ANCA, anti-dsDNA, anti-C1q and anti-nucleosomal antibodies. Antiphospholipid antibodies may also be present, which is responsible for the formation of blood clots in the blood vessels of the brain, heart or other organs, and which may cause recurrent miscarriages. In addition, leukopenia and thrombocytopenia are often found in the blood count.

Treatment: Treatment is by pulsed intravenous prednisolone for 5 to 7 days and then switched to oral glucocorticosteroids and immunosuppressants such as cyclophosphamide, azathioprine, cyclosporin A and mycophenolate mofetil.

b) GOODPASTURE TEAM

Is caused by the presence of IgG autoantibodies against the glomerular basement membrane. Characteristically, these antibodies cross-react with the proteins of the basement membrane of the alveoli.

Symptoms: Goodpasture's syndrome usually occurs in men under 40 and presents with bleeding from the respiratory tract (hemoptysis), which often precede the clinical picture of rapidly progressing glomerulonephritis. It happens that only the kidneys are affected by the disease process.

Diagnosis and treatment: It is based on the presence of antibodies to the glomerular basement membrane (anti-GBM) in the blood serum. In addition, linear deposition of these antibodies in the glomerular basement membrane and alveoli can be demonstrated by immunofluorescence testing of the biopsy. Goodpasture's syndrome differentiates from other pulmonary-renal syndromes such as Churg-Strauss syndrome, Wegener's disease, HUS syndrome and rheumatoid vasculitis.

Treatment: It is based on the use of plasmapheresis, pulse therapy with methylprednisolone (dose 500-1000 mg) and pulse therapy with cyclophosphamide (dose 1000 mg) once a month.

c) SCHONLEIN-HENOCH DISEASE

Henoch-Schӧnlein disease is a condition that mainly affects children, usually up to the age of 15.

Symptoms: It is characterized by the presence of skin haemorrhagic purpura (mainly inlimbs), joint inflammation, abdominal pain with gastrointestinal bleeding and symptoms of glomerular nephropathy. Symptoms of nephropathy include hematuria or hematuria associated with proteinuria, nephrotic syndrome, or rapidly progressive glomerulonephritis.

Diagnostics and tests: Established on the basis of characteristic clinical symptoms. In addition, serum levels of IgA and circulating immune complexes are increased.

Treatment: Only symptomatic.

2. Rapidly progressive glomerulonephritis

Rapidly progressive glomerulonephritis is a condition that leads to renal failure in the short term. If left untreated, it can cause uremia to develop within 6 weeks.

Reasons

The disease may be a spontaneous disorder or a renal symptom of a systemic disease (e.g. Wegener's Hodgkin). Based on serological tests, three types of rapidly progressing glomerulonephritis can be distinguished.

  • type I - in type I, it can be detected by immunofluorescence testing of an antibody against the basement membrane of the glomeruli or antibodies additionally present in the lungs (Goodpasture's syndrome). These are the so-called anti-GBM antibodies.
  • type II - type II is characterized by the presence of deposits of immune complexes in the glomerular basement membrane, which form characteristic clusters. Such a picture is found in lupus, post-streptococcal glomerulopathy and in cryoglobulin-induced glomerulopathy.
  • type III - in type III there is a picture of vasculitis with the presence of antibodies to the cytoplasmic antigen of granulocytes (c-ANCA). It is characteristic of Wegener's Hodgkin's disease, panenteritis microscopica and glomerulonephritis extracapilaris.

Symptoms

The sick have

  • significant arterial hypertension
  • large proteinuria
  • accelerated OB
  • increase in creatininemia

Diagnostics

Rapidly progressive glomerulonephritis differentiates from acute renal failure of pre-renal, atrophic, or acute interstitial nephritis. Serological tests and a kidney biopsy are used for the differential diagnosis.

Treatment

Treatment with plasmapharesis and glucocorticosteroids for 5 to 7 days. In addition, cyclophosphamide is added to the therapy.

Prognosis

The prognosis depends on the stage of the disease in which immunosuppressive treatment was initiated. InIn the case of preserved residual kidney function, it is possible to improve the function in half of the patients. Patients with type I of this disease usually do not relapse, unlike patients with rapidly progressing glomerulonephritis types II and III.

According to an expertIza Czajka, nutrition physiologist

Diet for kidney disease and proteinuria

What diet should be used for tubulointerstitial nephritis, proteinuria?

Iza Czajka, nutrition physiologist: In acute nephritis, a diet relieving the sick organ is used. Depending on the dynamics of the inflammatory process, your doctor should determine your diet.

General recommendations are for sodium and protein restriction. A carbohydrate-fat diet with very little s alt and fluid restriction is recommended. We serve rice gruels, rusks, a low-protein flour wheat roll, limited amounts of fruit puree, compotes, mashed potatoes.

Sample menu for about 1400 kcal: 1st breakfast - semolina with fruit puree. 2nd breakfast - biscuits, 200 ml of tea with sugar. Lunch - pure with butter, apple compote. Afternoon tea - a pumpkin and apple drink 200 ml, a small buttery roll. Dinner - rice gruel with butter, rusks.

As you recover, your diet is enriched with all products.

3. Chronic progressive glomerulonephritis

Chronic progressive glomerulonephritis includes the stages of development of various pathomorphological forms of glomerulopathy. Most patients have no acute onset.

Reasons

The essence of chronic progressive glomerulonephritis is damage to the glomeruli (phase I of glomerulonephritis). As a result of this damage, plasma proteins penetrate into the pramuria, which, reaching the lumen of the proximal tubules, stimulate the tubular cells to produce endothelins, chemokines and cytokines. This results in the proliferation of renal interstitial fibroblasts and the synthesis of extracellular matrix, as a result of which there is progressive fibrotization and hence renal parenchyma atrophy. In addition, glomerular damage has the effect of activating the renin-angiotensin system and increasing the production of angiotensin II. This, in turn, by increasing the synthesis of transforming growth factor beta, leads to the hypertrophy of tubular cells and their transformation into fibroblasts producing type IV collagen. In this way, the process of kidney fibrosis is even faster.

Factors accelerating the progression of nephropathy are the severity of proteinuria, the level of systemic pressure, the presence of toxinsendo- and exogenous as well as metabolic disorders such as diabetes, hyperlipidemia and disturbances of water, electrolyte and acid-base balance.

Symptoms

The disease remains asymptomatic for a long time. Its onset is difficult to establish, and it is usually diagnosed accidentally by the presence of proteinuria, hematuria, red cell rolleruria, and arterial hypertension in the patient. The disease progresses very slowly and leads to the development of uremia only after several years of duration. The symptoms of the patient largely depend on the degree of renal failure. Factors accelerating the disappearance of residual renal parenchyma include high and uncontrolled hypertension, water and electrolyte disturbances, hyperlipidemia, hyperuricemia, hyperglycemia or the use of non-steroidal anti-inflammatory drugs.

Treatment:

In patients with normal renal excretory function, it is recommended to use medications that lower blood pressure, anti-aggregation drugs and, if necessary, antibiotics. Any immunosuppressive treatment should depend on the type and activity of the glomerulopathy present. In addition, it is recommended to carefully control the water-electrolyte and acid-base balance and limit the supply of proteins. In the presence of hyperlipidemia, drugs that lower blood lipids are used, and in the case of hyperuricemia - allopurinol.

4. Chronic glomerulonephritis as manifested by isolated hematuria and / or proteinuria or intermittent hematuria

Reasons

Causes of hematuria with or without proteinuria include:

  • primary glomerulopathy (IgA nephropathy - Berger's disease, thin basement membrane disease, other proliferative segmental or focal glomerulopathy)
  • glomerulopathy in the course of a systemic or congenital disease (Alport-Fabry syndrome, sickle cell anemia)
  • glomerulopathy in the course of infections or haemorrhagic diathesis (deficiency of coagulation factors, angiopathies)

Diagnostics, tests

The diagnosis of the above-mentioned causes of haematuria can be difficult and can only be based on a careful examination of the kidney biopsy, exclusion of the urological cause of haematuria or blood coagulation disorders. The presence of dysmorphic erythrocytes in the urine may be very helpful in determining the cause of haematuria, which indicates their glomerular origin.

a) IgA NEPHROPATHY (BERGER'S DISEASE)

Berger's disease is an example of chronic glomerulonephritis that manifests itself periodicallyoccurring haematuria with coexisting infection of the upper respiratory tract, urinary tract or gastrointestinal tract. It is characterized by the presence of immune complexes composed mainly of IgA and C3 linked to exogenous antigens within the mesangium of the renal corpuscle.

Symptoms: Episodes of periodically appearing hematuria are not accompanied by any joint or abdominal pains or skin eruptions. After a few days, a rapid decrease in erythrocyturia can be observed, then it remains at a constant, low level until another attack of hematuria occurs.

Diagnostics, tests: It is determined on the basis of interviews and the result of immunofluorescence of the kidney biopsy.

Prognosis: About 50 percent IgA nephropathy may cause the development of chronic uremia in patients. It is worth remembering that in the presence of arterial hypertension and high proteinuria, disease progression is significantly accelerated.

Treatment: It depends on the clinical course and the amount of proteinuria. The use of glucocorticosteroids is indicated in patients with proteinuria above 0.5 g / day and the picture of glomerulonephritis microsopica in the bioptical examination of the kidney. If there are proliferative changes in the mesangium, it is recommended to administer the enzyme convertase inhibitors and AT-1 receptor blockers together with glucocorticosteroids.

In Poland 95 percent people with chronic kidney disease do not know about the disease

Up to 4.5 million Poles suffer from chronic kidney disease. To save lives, 4,000 people start treatment with dialysis. Most of them find out about the disease too late.

source: Biznes.newseria.pl

TUBEROCENTINARY KIDNEY INFECTION

Tubulointerstitial nephritis is a heterogeneous group of diseases caused by both non-infectious and infectious agents. Their course can be acute and chronic. The disease develops within the renal tubules and their supporting tissue (interstitial tissue) and is usually manifested by polyuria, tubular acidosis, renal s alt loss, and hypo- or hyperkalemia. In addition, patients suffer from proteinuria, moderate arterial hypertension, and anemia. It is worth remembering that the result of the inflammatory process in the interstitial tissue is the loss of the renal parenchyma and the development of uremia. Treatment is causal - if it is possible at all.

Reasons:

The main causes of interstitial nephritis are:

  • hereditary kidney disease (e.g. Alport syndrome, cystic kidney disease in adults)
  • exogenous (e.g. heavy metals, analgesics, some antibiotics) and endogenous (e.g.hyperuricemia, hypokalemia, cystinosis)
  • immune disorders (e.g. Sjӧgren's syndrome, amyloidosis)
  • disorders of kidney blood supply caused e.g. by atherosclerotic changes in renal vessels, acute non-inflammatory renal failure
  • infections
  • cancers (e.g. multiple myeloma, lymphomas)
  • other causes (e.g. obstructive nephropathy, vesicoureteral outflow)

1. Non-infectious acute interstitial nephritis

Non-infectious acute interstitial nephritis is a condition characterized by edema and cellular infiltration of the interstitial tissue. It can be caused by factors that impair renal blood flow, drugs, endogenous and exogenous toxins, and immunological reactions.

Symptoms

They depend on the etiological factor and the intensity of changes in the renal tubules and interstitium. In acute interstitial nephritis caused by endogenous or exogenous toxins or in infectious diseases, symptoms of kidney damage usually occur from the beginning of the disease, while in acute interstitial nephritis due to hypersensitivity to drugs, symptoms may appear immediately after taking the drug or only after taking the drug. some time (usually a few weeks) after taking them. In the case of acute interstitial nephritis of immune etiology, it is found in patients:

  • fever
  • rash
  • joint pains

In addition, they have peripheral blood eosinophilia, biochemical features of liver damage, increased creatininemia and urea concentration, and acute metabolic acidosis. Renal symptoms of this type of nephritis can include moderate proteinuria, hematuria, rolleruria, and leukocyturia, as well as oliguria or anuria. It is worth remembering that usually after the causative agent of acute interstitial nephritis has expired, all symptoms of nephropathy disappear.

Diagnostics

The diagnosis of acute interstitial nephritis is usually easy, and only some patients require a kidney biopsy for diagnosis. The disease should be differentiated from acute glomerulonephritis and from acute pyelonephritis.

Treatment

Treatment of acute interstitial nephritis is causal. For example, if it is suspected that it is caused by medications taken by the patient, these medications should be discontinued. In acute immune-mediated interstitial nephritis, short-term administration of glucocorticoids is recommended.

2. Chronic non-infectious interstitial nephritis

Chronic interstitialNon-infectious nephritis is a disease characterized by the presence of cellular infiltrates in the interstitial tissue that lead to fibrosis and destruction of renal structures.

Reasons

The causes of this type of inflammation include:

  • metabolic disorders such as diabetes, hypercalcemia, hyperuricemia
  • poisoning with heavy metals, e.g. lead, cadmium
  • drugs such as paracetamol, salicylic acid derivatives, lithium s alts or cyclosporine A
  • immune reactions occurring, for example, in patients after kidney transplantation

Symptoms

The course of the disease is asymptomatic for many years. Initial symptoms include polyuria, nocturia, and impaired urine concentrating. In addition, patients with chronic interstitial nephritis are highly susceptible to bacterial infections, which means that they often develop bacterial pyelonephritis. The development of infection accelerates the progression of nephropathy.

Diagnostics, tests

The diagnosis of chronic interstitial nephritis is very difficult due to the fact that many patients hide the constant intake of painkillers. It is important to carefully take the history and perform diagnostic tests to detect possible metabolic disorders. The disease is differentiated from chronic (bacterial) pyelonephritis and chronic glomerulonephritis.

Treatment

Treatment is based on removing the causative agent of the disease, combating the accompanying bacterial infections of the kidneys and arterial hypertension.

Diabetes destroys kidneys

source: Lifestyle.newseria.pl

3. Infectious interstitial nephritis

Infectious interstitial nephritis is a disease in which inflammation takes place in the interstitial tissue of the kidneys. They are caused by either ascending urinary tract infections or blood-borne infections.

Reasons

The most common pathogens responsible for bacterial urinary tract infections are Escherichia coli, Psuedomonas aeruginosa, Proteus vulgaris, and Klebsiella. In addition, bacterial settlement is favored by renal ischemia, some metabolic disorders such as diabetes or gout, overuse of non-steroidal anti-inflammatory drugs and the use of immunosuppressants. Infections result in impaired renal tubular function and damage to the renal parenchyma, which leads to its fibrosis and scarring. It is worth remembering that acute infections can lead to abscess formationlocated between the cortex and renal papillae, while chronic infections result in complete renal fibrosis.

ACUTE AND CHRONIC MODELIC KIDNEY KIDNEY

Symptoms of acute pyelonephritis

Characteristic is fever with chills, dysuria, and tenderness and pain in the lumbar region. The symptoms seen in children may be unusual - there is fever, abdominal and headaches, nausea and vomiting. It is worth remembering that acute pyelonephritis can result in the development of multiple renal or perirenal abscesses and the development of severe sepsis.

Symptoms of chronic pyelonephritis

It is worth remembering at the outset that chronic pyelonephritis develops only in patients with changes in the urinary tract that impede the outflow of urine. The symptoms are usually non-specific and include:

  • general weakness
  • headaches
  • nausea
  • weight loss
  • pains in the lumbosacral region

In addition, there are low-grade fever or high blood pressure. If it is not possible to remove the obstacle in the outflow of urine, hydronephrosis or pyonephrosis develops, which leads to the complete disappearance of the kidney parenchyma and the development of uremia.

Diagnostics, treatment

The diagnosis of acute and chronic pyelonephritis is based on a detailed history and diagnostic tests such as blood count, urine, ultrasound, urography and computed tomography. Do not forget to perform a prostate examination in men and a gynecological examination in women.

  • Blood morphology - for acute pyelonephritis, it is typical to accelerate the precipitation of red blood cells and increase the number of white blood cells. Anemia and an increase in creatinine and / or urea concentration are observed in patients with chronic pyelonephritis. In addition, there may be disorders in urine concentrating and features of tubular acidosis
  • Urine test - the presence of leukocyturia indicates inflammation in the urinary tract, while the white blood cells indicate pyelonephritis. Moderately severe erythrocyturia is found in both acute and chronic pyelonephritis. In addition, the proteinuria present is small and is mainly tubular in nature.
  • Ultrasound examination (USG) - is particularly useful in the diagnosis of chronic pyelonephritis. The examination shows that the contours of the kidney are tightened,thinning of the kidney cortex and distortion of the calico-pelvic system resulting from the destruction of the kidney papilla and the presence of scarring changes.
  • Urographic examination - in the case of acute pyelonephritis, this examination does not show particularly characteristic features, while in the case of chronic pyelonephritis, there are distortions of outlines and the phial-pelvic system and uneven thinning of the cortex

Pyelonephritis is differentiated from primary or secondary glomerulopathies, cancers of the urinary and genital tract, and abdominal organ conditions such as appendicitis, pancreatitis, and gallbladder inflammation.

Treatment: In the case of acute inflammation of the urinary tract, the most important thing is to remove the causes that obstruct the outflow of urine or the factors that predispose to urinary tract infections. It is important that the choice of antibiotic is based on the determination of the causative organism and its susceptibility to different antibiotics. Typically cotrimoxazole, amoxicillin or quinolone derivatives are used for a period of about 5 to 7 days. It should not be forgotten that when choosing and dosing an antibiotic, the degree of impaired renal excretory function should be taken into account and that possible hypersensitivity to these drugs should be ruled out.

Treatment of chronic pyelonephritis is causal. In the event of an infection, the selection of an antibiotic should be based on the antibiotic result, and treatment should be continued until all symptoms have disappeared. In addition, one should not forget about the treatment of arterial hypertension with convertase inhibitors, sartans and non-dihydropyridine calcium channel blockers. Erythropoietin is used in the presence of anemia.

Prognosis:

With the elimination of factors contributing to the development of pyelonephritis, the prognosis is good, provided that antibacterial treatment is implemented early. In the remaining patients, the disease may be prolonged and lead to a gradual reduction of the active renal parenchyma and the development of uremia. The progress of nephropathy can be slowed by treating exacerbations of inflammation and hypertension, as well as by avoiding fluid and electrolyte disturbances and limiting protein intake.

Category:

Urology and Nephrology