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Oliguria

Oliguria is called an insufficient urinary volume to eliminate toxic waste from the body, generally less than 400 ml daily in an adult weighing 70 kg.

Anuria

Absence of urinary flow, mainly caused by obstruction of the urinary tract or obstruction in the arterial or venous renal tree. There are parenchymal diseases that can also cause absence of urinary flow, such as cortical necrosis or rapidly progressive Glomerulonephritis but much less frequently than the previous causes, so obstructive causes must be ruled out before thinking of another etiology.

Uremia

Plasma urea and creatinine concentrations are measured to assess glomerular filtration. Both substances are constantly produced in the liver and muscles respectively. These substances undergo complete glomerular filtration and are not reabsorbed in large quantities by the renal tubules, so their clearance tends to be a reflection of glomerular filtration. When it falls, an increase in its serum concentrations occurs, leading to a state of uremia or hyperazoemia. Creatinine is a more reliable index of glomerular filtration than urea, due to the lower back diffusion of the latter from the tubular lumen to the peritubular blood. Glomerular filtration can be reduced by a decrease in the filtration of individual functional nephrons or by a reduction in the number of them.

REDUCED GLOMERULAR FILTER IN EACH NEPHRON

When there is a decrease in extracellular volume, a significant response is generated in the normal kidney, characterized by a reduction in the glomerular filtration of each nephron and the subsequent reabsorption of sodium chloride (ClNa) and water that reaches the tubules. . The resulting hyperazoemia is called prerenal, and in it the urinary concentration of Na falls below 20 meq / l. Vasopressin secretion (ADH) is stimulated by reduced volume of extracellular fluid volume, and consequently the distal tubules and collecting ducts become fully permeable to water. The concentrating mechanisms of the renal medulla are very effective when the flow through the Henle loops and collecting ducts is low. Due, the filtrate that escapes reabsorption in the proximal tubule suffers a maximum osmotic concentration, the urine volume is small and has a high osmolarity, greater than 500 mosmoles per Kg of water. Most of the filtered creatinine escapes tubular reabsorption, and consequently the ratio between urinary and plasma creatinine concentrations (U / P) is very high, 40 or higher. Because urea diffuses retrograde more than creatinine, blood urea nitrogen (BUN) levels are higher than serum creatinine. Normally the ratio between BUN and serum creatinine is 10: 1; with the reduction of extracellular volume this proportion increases. There are other situations where this relationship can be altered such as treatment with tetracyclines, treatment with corticosteroids,

Table 1. Pathophysiological Mechanisms of Prerenal Hyperazoemia

Prerenal hyperazoemia can appear in any edema-forming process during the ClNa and water retention phase. Typical examples are nephrotic syndrome and liver cirrhosis with ascites. When a diuretic is administered in these cases, the urine volume and concentration of Na may be normal, but upon removal, the Na and water retention mechanisms are reactivated, again giving rise to a state of oliguria. Prerenal hyperazoemia may also be seen when renal blood flow is reduced due to systemic hypotension, incomplete occlusion of the renal artery or vein, or other cause.

Certain acute kidney diseases that cause hyperazoemia decrease the glomerular function of each nephron and at the same time injure the tubules enough to reduce and even abolish their reabsorptive function, producing an ARF. Acute tubular necrosis (ATN), nephrotoxic agents, and acute tubulointerstitial disease are excellent examples. Hyperazoemia and oliguria appear but the urinary Na concentration exceeds 20 meq / l and usually 40 meq / l.

REDUCTION OF THE NUMBER OF NEPHRONS

Depending on the function of each nephron, we can see three types of situations:

1. Glomerular filtration of each increased nephron
   
   If one kidney is removed, the other experiences an increase in size at the expense of an increase in the size of its nephrons (hypertrophy) and thus increases glomerular filtration, approaching the normal GFR provided by two kidneys. The tubules are overperfused with filtration, but withstand the reabsorptive load. If more nephrons are removed from the single kidney, the remaining nephrons further increase the size and thus the GFR. In this case, hyperazoemia appears because despite increasing the size of the remaining nephrons, the overall GFR is low. The conservation of water and Na are lower, so a higher intake must be ensured. The clinical conditions that produce this condition are the surgical loss of the renal parenchyma secondary to trauma, malignancies, lithiasis and destruction of the parenchyma due to bacterial infections or tuberculosis.
   
   
2. Glomerular filtration of each normal nephron. The glomerular function of each nephron does not appear to increase despite the reduction in the number of nephrons in diseases such as Glomerulonephritis and Diabetes (DBT) glomerulosclerosis, in which the glomerulus is the main site of injury. In these diseases, the total GFR decreases in direct relation to the number of nephrons and is not maintained by an elevation of glomerular function in each nephron.
   
   The conservation of sodium and water is conserved by little tubular damage. Oliguria can be observed with low urinary sodium concentration. The urea / creatinine ratio rises markedly.
   
   
3. Glomerular filtration of each reduced nephron

In patients with chronic kidney disease in whom the total GFR has been sufficient for life support only at the expense of glomerular filtration in each increased nephron, inadvertent dehydration or any other factor that decreases the filtration for each nephron can cause oliguria and intense hyperazoemia.

Table 2: Reduction of the number of nephrons

DIAGNOSIS OF HYPERAZOEMIA

The finding of a high concentration of nitrogenous products and / or a decrease in urine output forces the doctor to initiate a deductive process that allows him to discern the type of kidney failure he is facing and, if possible, the noxa that causes it. To do this, they will resort to a staggered process of exclusion based on the completion of a comprehensive medical history, which includes a careful anamnesis of the patient's personal history, a meticulous exploration and the weighted and sequential use of complementary tests.

While the syndromic diagnosis of kidney disease is relatively simple, the etiological diagnosis on which the effective treatment of the patient depends is often difficult. Therefore, we recommend analyzing the following reflections:

1. The causes that can produce kidney failure are very diverse. Alteration or damage of any of the kidney structures (intrarenal vessels, glomeruli, tubules and interstitium) can produce parenchymal IR. Likewise, factors unrelated to the kidney itself but which alter its hemodynamics (prerenal factors) or prevent the elimination of urine (postrenal factors) can cause it.
   
   
2. Kidney failure in men is often multifactorial. For example, volume reduction, low expenditure, and nephrotoxicity may be coexisting causes in acute tubular necrosis (ATN).
   
   
3. Acute kidney failure is a dynamic process that can evolve to more serious stages. Thus, a prerenal failure can evolve to parenchymal if the injury is sustained and cause an ATN.
   
   
4. There is never a need to resort to a diagnostic "storm", carrying out multiple analyzes and complementary explorations, but rather that the diagnostic procedures must be staggered, based on their efficacy and safety for the patient.

Chronic Renal Insufficiency (CRI) VS Acute Renal Insufficiency (ARI). SIGNS AND SYMPTOMS

Sometimes the distinction between these situations is difficult. The first point to investigate is the possible existence of previous analytical controls of renal function obtained in routine examinations or in previous pathological processes, which will allow us to know if the current deterioration is acute or chronic. The existence of a history of previous kidney disease will suggest an evolution of the process towards CRI. It should also be borne in mind that a patient with Chronic Kidny Disease may have an acute deterioration similar in origin to that of a healthy subject, or due to an outbreak of his underlying disease. The analytical controls after detecting an elevation of the nitrogenous products are very indicative: in the CRI, the values ​​remain constant, while in the IRA daily increases are often observed, more than 0, 5 mg / dl in plasma creatinine. In the absence of previous data on kidney function, the patient's symptoms are very useful. Uremic syndrome, characterized by asthenia, anorexia, drowsiness, cramps, morning sickness or vomiting, polyuria or polydipsia of long evolution indicate a chronic process, rare to see in the ARF. It is also possible to find the ureochrome dye of the skin, which must be differentiated from jaundice, also present in a long-standing process. The presence of well-tolerated anemia, hypocalcemia and hyperphosphatemia or metabolic acidosis also leads us to think of a chronic process (but it can also be seen in an acute process with a little more time of evolution). Regarding complementary methods such as renal ultrasound,

SUPPLEMENTARY TESTS

Blood and urine measurements of sodium, potassium, osmolality, urea and creatinine, with which different diagnostic indices can be established, constitute an important aid in the diagnosis of hyperazoemia. Fractional excretion of sodium: EFNa = (NaU x CrP / NaP x CrU) x100 which has the highest sensitivity and specificity to diagnose the type of acute renal failure. In general, values ​​lower than 1 suggest a prerenal origin, while those higher than 2 would be seen in ATNs. Occasionally, intermediate EFNa values ​​between 1 and 3 can be seen in tables where a number of nephrons are in the prerenal stage and respond to expansion with fluids, and others have ATN, which keep urea and creatinine levels high.

Another valuable test in daily practice is urinary sediment. In ATNs, it usually shows only granular and / or hyaline cylindrics of brownish coloration, due to cellular debris of the tubular epithelium and the presence of Tamm-Horsfall protein, scaly tubular cells. In the prerenal IR the sediment is normal. In the presence of dysmorphic hematuria, cylindruria, leukocyturia, we are facing an IR of parenchymal etiology. Wright staining should be used to diagnose eosinophiluria if we suspect tubulointerstitial nephritis. The observation of calcium oxalate crystals is seen in poisonings by ethylene glycol, methotrexate or methoxyflurane. Those of uric acid in tumor lysis.

OTHER COMPLEMENTARY METHODS

Ultrasonography: The normal renal size (10-12 cm) is decreased in CKD, except in polycystosis, myeloma, amyloidosis and DBT in non-terminal stages.

In acute parenchymal processes it is possible to observe increased echogenicity but it is nonspecific. Large kidneys may be seen due to edema of the renal interstitium (NTIA, lymphoma, vasculitis, and GNF).

An increase in kidney size can be seen in obstructive processes where we would see pyelocaliceal dilation. When the obstruction occurred in the last 24 to 48 hours, dilation may not be seen yet, so the study should be repeated. In this case, a conserved corticomedullary thickness (2 cm) speaks of an acute obstruction.

Doppler ultrasound: evaluates the renal vasculature and rules out pathology at the level of large and medium vessels (stenosis, dilation, embolism, etc.).

Plain abdominal radiography: Provides information on renal morphology, presence of lithiasis and vascular calcifications.

Computed Axial Tomography: Useful for obstructive pictures and their causes. Pyelonephritis.

Isotopic Studies: Of little use in kidney failure.

Renal Biopsy: It is only useful in suspected renal failure due to glomerulopathy, or when the IR lasts despite the treatment established according to the initial suspicion diagnosis.