• histologic lesions were mainly localized in the glomeruli,
• Evolution is a long, progressive and usually ends with irreversible renal failure.
The types of diseases:
• In terms of clinical
Oligosymptomatic forms of proteinuria. hematuria, anemia as isolated symptoms.
Eden form, a form of hypertensive, with renal insufficiency forms, forms with more or less represented all the syndromes of renal disease.
• In terms of etiology
Most are of unknown origin. In a few cases, there is a period of acute renal disease in the past.
The secondary glomerulonephritides: The primary disease may be disseminatus lupus erythematosus, rheumatoid purpura, amyloidosis, diabetes mellitus. Sometimes it is due to the toxic effects of medications - sulfonamides, kanamycin, antineuralgičnih funds.
• In terms of anatomical
In cases which are due by the end of their evolution kidneys are small, sclerosated. There is a strong interstitial fibrosis. Changes in the blood vessels in the form of arteriosclerosis obliterans and arteriolonekroze angeitisa.
• The functional
The reduction in glomerular filtration rate, decrease in renal blood circulation, reduction of tubular function, which corresponds to more global reduction of renal function, with greater or lesser impairment of certain partial functions of the nephron.
Diagnosis
Anamnesis
Rarely has the data on the acute glomerulonephritis. The most common problems were fatigue, headache, polyuria, nikturija, increased thirst, anemia, dyspnea effort. In severe cases, failure to join uremic signs: Anorexia, Nausea, intermittent or constant vomiting, hiccups, weight loss, bleeding.
The clinical picture
Long time without interference, without clinical findings. Diagnosis is made on the basis of laboratory tests of urine and blood. Sometimes edema, hematuria, signs of cardiovascular disease to make an introduction. In the course of evolution may be acute strokes with lumbar pain, puffy face in the morning, swelling of the ankles at night. Color is a pale face. Blood pressure normal or elevated. Edema volatile.
Nekiput nephrotic syndrome, changes in heart and retina in relation to hypertension.
At an advanced period sivožućkasta color. There is dyspnoea of effort. Often heavy bleeding from the nose. Ammonial halitosis. Even with strong ezotemijom some are able to do their usual job. The situation is still very unstable, so that of any intercurrent disease, infection, trauma, surgery, gastrointestinal disorders, bleeding, complications of the heart can be translated into a period of thermal failure.
Edema are common in the secondary glomerulonephritis in the emiloidoze, diabetic glomerulosclerosis, nephropathy pregnant women, lupus erythe, so called. nefrozo-nephritis.
As it progresses, there are all the signs and symptoms, as in uremia - the differences are quantitative in nature, and there are all transitions.
Laboratory tests
Sometimes the disease is first detected during a systematic examination of urine.
Proteinuria is a consistent finding. It may be a trace, but a few grams in 24 hours. In nephrotic syndrome prevalent serum albumin, beta and alpha two globulins fast, while the gamma globulins are present only in trace amounts. In cases of severe lesions of glomerular capillaries is non-selective proteinuria, with a proportionately greater amount of globulin. In the terminal phase reduces the intensity of proteinuria, and then all belančevinske serum fractions proportionally represented. There are cases with proteinuria long time the only finding.
Hematuria is almost obligatory finding. It has a momentum of disease with macroscopic hematuria.
In the late period of the disease can disappear. There are forms with hematuria as the only sign of disease. In these cases, only renal biopsy can elucidate the nature of the disease.
Leukocyturia was frequently increased.
Hyaline and granular cylinders are often found.
The concentration of urea in the blood is gradually increasing. For a long time may be within normal limits. Additions are different degrees, there are signs of uremia regularly when the blood urea was 300 mg%.
Total non-protein nitrogen increased in parallel with uremia.
Uric acid is increased, but proportionally less than urea.
Creatinine increases in proportion to the increase of urea.
Global aminoacidemija usually not changed, but some amino acids can be increased, others decreased.
Polypeptides were not elevated.
Possible disturbances in the balance of salt and water, but not specific to chronic glomerulonephritis.It has a form with a uri-plenary losses of sodium, potassium, but less frequently than in pyelonephritis.
Hypocalcaemia is common, and the reduction of bicarbonates in the blood.
Functional testing
There are various options, from fully preserved functional capacity to a global failure. It is characteristic that predominates in the earlier stages of damage to glomerular filtration. In later periods resulting damage and tubular function.
There is the case with the outage of only certain tubular function: loss of sodium, potassium, water, amino acids, the inability of acidifying urine.
Radiology
Nativan clip: reduction in cases of kidney nefroskleroze.
lv pyelogram: depending on the degree of failure, the picture is normal, pale with the late appearance of contrast, or negative, if the values of urea increased.
The sequence of signs, symptoms, according to the parameters of significance for the diagnosis
Anamnesis
General weakness, anemia.
Clinical findings
Urinary Syndrome, a constant of proteinuria, hematuria. High blood pressure. Changes in the retina.In the advanced periods of the disease - azotemički syndrome.
The functional state
Reduction in clearance of urea, creatinine (not constant) the inability of the concentration of urine, reduced PSP excretion, decreased urine acidification ability (impairment of global renal function).
Functional characteristics of
Chronic glomerulonephritis is accompanied by changes in functional status. It is harder to damage the glomerular filtration, but in other functions.
With advances dektruktivnog process reduces the number of nephrons is capable of function.Dysfunction then transform in the sense that the function corresponding to the reduced body weight in the functional: fixing the level of specific gravity and izotonije izoosmije plasma, the appearance of abundant diuresis, enhancement of blood urea and its progressive increase in parallel with the progress of the destructive process. So, it's not about the damage some of the partial functions, but the reduction of global renal function.
Special types of diffuse glomerular lesions, or with extra capillary proliferative changes can quickly lead to severe HF. Then it is impossible to distinguish what is proizrokovano insufficient glomerulus function, and what reduction in the number of nephrons.
It is not global but partial kidney failure.
It is not global but partial kidney failure.
Forms and oligo monosimptomatski may be the only sign of illness:
• The minimal urinary findings (proteinuria light alone, or with microhematuria).
• Excessive urinary findings: heavy proteinuria, micro-and macro-hematuria. No hypertension, or damage to the concentration of urine.
• Urinary findings of minimal or profuse, with izostenurijom - there is renal insufficiency, without uremia.
• Renal failure with uremia. Compensated period: blood urea increased, but at the same conditions of nutrition, physical activity and hydration of urea remains a long time on the same level and slowly increasing, it is usually abundant diuresis, over 1.5 liter for 24 hours and obligantna is
that. can not reduce the limit of drinking water.
• Decompensated renal failure - uremia. If associated with hypertension, quickly establishing decompensation. Each stage in the evolution of the disease is shorter, if blood pressure is elevated.
In functional terms, there are stages with preserved function of excretion of nitrogen compounds, the first two phases, then phase which is characterized by reduced urine concentrating ability, and still preserved the ability of excretion of nitrogenous compounds - the third stage. The blood urea is elevated. However, if you are working clearances, they are decreased, indicating that the funkcionilna weight decreased. Finally, when the stage is caused by increased excretion of urea in the blood of its value, the fourth stage - the period offset by uremia and finally, the fifth stage when the kidneys are not able to maintain homeostatic systems of the body.
The minimum program for functional testing:
First Concentration test (in addition to standard qualitative analysis of urine).
Second Clearance of urea.
Third Creatinine clearance.
4th PSP testing.
5th Addis's number - for orientation in terms of evolutionary traits.
Measuring the clearance of urea, creatinine, and the determination of PSP concentration probe gives insight (if it is repeatedly determined at specified intervals) and is currently working state, and the remaining body reserves, as well as the evolutionary characteristics of kidney disease (a comparison of successive values).
For special cases it is necessary to determine the titre of acid, the excretion of NH4 ions, an index of sodium or potassium excretion, in order to assess whether there are relatively greater damage to tubular function than glomerular filtration.
Forecast
For the assessment of prognosis is needed to determine:
1) Is the issue of chronic glomerulonephritis, chronic pyelonephritis, or various nefroangioskleroza
urological diseases.
2) Is the disease is evolving, cured, inpatient, or progressive.
It's hard to say when and that there is a cure if certain findings are maintained.
The criterion of cure
The clinical picture decisions. The urinary findings are minimal. There is no edema. If there is hypertension, it does not necessarily mean that the process is evolutionary, esencijelna hypertension was common (Renbi). Decide the value of clearance: if they remain normal for several years, little seems that the process will lead to kidney glomerular sclerosis. Or if the pathological values of clearance in the further course of normal and such stay next year, then this only in terms of evolution toward healing.
Normal values vary much clearance, so that in one case clearances may be on the average, yet the normal range, but we do not know whether they are normal for him.
In deciding such cases the test results later by comparing these values, whether those values decrease or remain the same.
For pyelonephritis decide: pyuria, bacteriuria, febrile periods, leukocytosis, abnormal images urographies, the presence of Sternheimer's cells in the urine.
For nefroangiosklerozu characteristic: pletoričan of a patient, familial occurrence of hypertension, hypertrophy of the heart, coronary insufficiency, generalized arteriosclerosis. No Sternheimer's cells, no bacteriuria, edema (not cardiac), dysuric disorders, anemia, anorexia, weight loss.
In some cases it can decide only the histological criteria - kidney biopsy.
In the course of evolution can occur with strokes worsening signs of acute glomerulonephritis edema, hypertension, proteinuria, heart failure. The most common sign of deterioration is increasing rapidly hematuria. These acute strokes sometimes contribute to the progressive deterioration of renal functional status, because the damage that they cause these evolutionary momentum, are not always fully reparabilne nature.
Vaccinations can cause acute deterioration of diseases that can give irreversible nature of the lesion and thereby contribute to a faster evolution of the disease.
Pregnancy can worsen with hypertension and renal insufficiency, and preeklamptičkim eklamptičkim attacks, death of the fetus or premature birth. In clinical terms there is a picture toxemia gravidarum, except that after termination of pregnancy does not occur normalization, it remains difficult glomerulonephritis. Kidney damage in that the more severe if blood pressure is higher and harder sudovne lesions.
Rapid evolution can predict if any:
• progressive reduction of the value of clearance,
• occurrence of hypertension and its rapid deterioration,
• progressive changes in the retina,
• formation of nephrotic syndrome,
• types of histological lesions type ekstrakapilarnog glomerulitisa proliferation.
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