Definition
Acute renal insufficiency (ARI) is defined as a rapid decline in renal function, characterized by increasing azotemia (which is best measured by serum creatinine) and may or may not be accompanied by oliguria. This sudden decline in renal function manifests itself within hours to days and results in failure, inability to excrete nitrogenous waste from plasma and maintain normal volume and electrolyte homeostasis.
Epidemiology, incidence
ARI is a common problem in current medical practice and in urology in hospitalized patients. Studies show that 2 % to 5 % of all patients admitted to the surgical department will have a developed ARI. The incidence can increase up to 20 % at ICU and after cardiovascular and abdominal procedures. The development of ARI is associated with a significant increase in morbidity and mortality. Therefore, it is important that the symptoms are recognized in time, a prompt diagnosis is made and subsequent complications are resolved.
Etiology
It is diverse. The most common conditions are associated with renal hypoperfusion, obstructive uropathy, the kidney parenchyma itself, acute glomerulonephritis. Significant renal ischemia occurs during massive bleeding, cardiogenic shock, and surgery. Hypoperfusion can cause both reversible and irreversible changes. ARI can also be caused by several nephrotoxic substances, e.g. heavy metals, organic solvents, contrast agents used in X-ray examinations of the kidneys and urinary tract. ARI also penetrates when a large amount of myoglobin is released into the circulation, rhabdomyolysis caused by trauma -crush syndrome, non-traumatic rhabdomyolysis in heat shock, extreme physical exertion.
Classification
From a pathogenetic point of view, we divide ARI into tubular and vascular. In the case of tubular failure, the cause is considered to be cylinders and waste, which prevents the outflow of urine. The pressure in the tubules increases and this is transferred to the glomeruli, where it inhibits or completely stops the filtration. In the vascular form, significant constriction of afferent arterioles - nerve stimulation, angiotensin II, or catecholamines is expected. Thus, the decrease in glomerular filtration rate (GF) dominates. Clinically, it is appropriate to divide the causes of ARI into 3 main categories - prerenal, renal and postrenal.
Prerenal ARI
It is caused by transient renal hypoperfusion, which can cause a decrease in GF. Return of renal function to baseline within 24 to 72 hours is usually considered a prerenal disease. Under normal circumstances, the kidney can maintain normal renal blood pressure and reduce GF to perfusion pressures of approximately 60 mmHg. The phenomenon of autoregulation requires a complex of interactions of physiological factors. In some hospitalized patients with impaired autoregulation, a decrease in blood pressure and a decrease in GF may result in a noticeable decrease in systemic blood pressure. When renal perfusion is impaired, angiotensin II and vasodilating prostaglandins play an important role in establishing glomerular hydrostatic pressure and GF. There are 3 major determinants in GF, including plasma renal flow, glomerular hydrostatic pressure, and glomerular permeability. Angiotensin II preferably has a greater vasoconstrictive effect on the efferent than on the afferent arterioles, where vasodilating prostaglandins cause vasodilation of the afferent arterioles. Drugs that block angiotensin II synthesis (ACE inhibitors), angiotensin II receptor antagonists, or prostaglandin synthesis inhibitors (non-steroidal anti-inflammatory drugs) may in some cases cause ARI. Prerenal azotemia can be encountered in patients with volume overload and also with decreased circulatory volume. Deficiency results from renal and extrarenal losses and results in systemic hypotension and renal hypoperfusion. Prerenal azotemia may also occur in a high degree of bilateral renal artery stenosis or in a state of renal hypoperfusion due to redistribution of extracellular fluid with peripheral vasodilation, e.g. sepsis.
Renal ARI (intrinsic)
The main causes of ARI include: - acute glomerulonephritis (finding: proteinuria, hematuria), - acute interstitial nephritis (finding: sterile pyuria, leukocytes, eosinophils), - acute tubular necrosis
Postrenal ARI
Caused by obstruction of the excretory system. Both kidneys may be affected or the dysfunction is solitary. We distinguish: = ureteral obstruction - extraureteral (tumor, fibrosis), - intraurethral (blood clots, uric acid crystals, stones), = bladder discharge obstruction (prostate hypertrophy), = urethral obstruction.
Pathogenesis of ARI
Not known in detail. The renin-angiotensin-aldosterone (RAA) system plays an important role. Its increased activity results in a decrease in blood flow and a decrease in GF, resulting in the development of an oligoanuric stage with uremic syndrome. Insufficient feedback to GF results in extreme polyuria and dehydration.
Clinical picture
It takes place regardless of the underlying cause of certain characters terrorist stages:
= initial stage - begins shortly after the onset of the causative agent and lasts until the onset of the first symptoms. In case of circulatory failure, this stage lasts several hours, in case of total infections 1-2 days, in case of poisoning 6-7 days. Symptoms of the underlying disease predominate. Circulatory failure develops anemia, dehydration, later general weakness, nausea, vomiting, diarrhea, abdominal pain, headache, jaundice, itchy skin, joint and muscle pain, and shortness of breath. At the end of the initial period, diuresis begins to decrease, and urea rises in the serum.
= oligoanuria stage - lasts several hours to several weeks. If the oliguria lasts more than 4 weeks, we consider a diagnosis of acute tubular necrosis, but also diffuse cortical necrosis, rapidly progressing glomerulonephritis, or renal artery occlusion. In anuria, diuresis is reduced below 100 ml/day. The specific gravity of the urine is reduced to 1010 and the osmolality to 300 mmol/l. Urine contains erythrocyturia, leukocyturia, cylindururia and proteinuria (1 to 15 g/day). The finding of Ehrlich-positive substances and bilirubin in the urine testifies to the current liver damage. Catabolism caused by fever, sepsis or extensive trauma is associated with high daily increases in serum urea and creatinine. Metabolic acidosis is an accompanying feature of ARI, both for increased production of acidic products and for their reduced excretion. It is manifested by deepened Kussmaul's breathing, headaches, meningeal symptoms and even coma. In catabolic processes in the body, the volume of metabolic water increases by more than 1 liter in 24 hours. Hyperhydration of the patient causes general swelling, which is manifested mainly by uremic swelling of the lungs. The breakdown of intracellular proteins is the cause of increased potassium, magnesium, sulfates and phosphates. One of the most serious consequences of ARI is hyperkalaemia, as a result of decreased renal potassium excretion and continuous release from tissues. It is asymptomatic up to values of 6.0 to 6.5 mmol/l, above these values it manifests itself in changes in the ECG image - bradycardia, high spiked T wave, QRS enlargement and prolongation of the PR interval. At higher values, there is a risk of cardiac arrest.
= stage of polyuria, early and late diuresis - the patient, after overcoming the oligoanuric stage, enters the stage of early diuresis when he starts to urinate about 500 ml/day, but the values of nitrogen catabolites and urea increase even more. In the late diuresis stage, the azotemia decreases until it resolves. Uremic syndrome subsides and diuresis increases. This stage is characterized by polyuria due to the inability of the tubules to resorb osmotically active substances in sufficient quantities. There is a risk of hypokalaemia, loss of NaCl and water. There is protein in the urine, casts and it isostenuria continues. This stage lasts 6-10 days. During this period, patients are prone to infections, especially of the respiratory and urinary tract. The return of renal function to normal values takes from a few weeks to 1 year. Mortality ranges from 30 to 60 %.
Diagnosis and differential diagnosis
ARI should be distinguished from chronic renal insufficiency (ChRI - chronic renal failure). ChRI is evidenced by a history of kidney disease, pallor, muscle atrophy, skin pigmentation, retinopathy, low back pain, heart enlargement, diastolic hypertension, pericardial friction, swelling, uremic breath and small kidneys on an X-ray image, irregular in shape. Percutaneous renal biopsy in the oligoanuric stage is important in the differential diagnosis of ARI. Ultrasonography (USG), native imaging, scintigraphy, angiography, CT are important of the auxiliary examination methods.
Therapy
It should focus on treating the cause of the disease. Prerenal ARI - perfusion correction usually solves the problem, treatment of shock, stopping bleeding, replenishment of blood volume. Elimination of nephrotoxic drugs, administration of an antidote in some poisonings will solve the issue of renal causes of ARI. Postrenal form of ARI - obstruction in the drainage system requires drainage. To reduce catabolism, amino acids and 100 g of glucose are given daily. Anabolic androgens are also administered to reduce catabolism. The toxic effects of hyperkalaemia can be influenced via iv. administration of calcium. Antibiotics at the oligoanuric stage to manage possible infection should be administered in a targeted manner, according to microbial sensitivity and in reduced doses, for reduced renal function. Diuretics increase diuresis, thus promoting the leaching of waste, pollutants and cylinders. Mannitol - increases blood flow to the kidneys, urine production, reduces cell edema, elimination of free radicals. The aim of the therapy is to prevent further damage to the renal parenchyma, to ensure nutrition, metabolic balance and to improve renal function, to optimize volume.
Prevention
This mainly concerns operations with the use of contrast agents - it is important to hydrate the patient and use non-ionic contrast agents.