Precipitaciones de calico, urato o cistina

Patients with acute renal failure are more likely to develop edema, hyponatremia, and
hyperkalemia due to sodium, water, and potassium retention

The intrarenal adaptations that allow the maintenance of fluid and electrolyte homeostasis are
more likely to occur with chronic (long-standing) renal disease

increase in the plasma creatinine concentration of at least 0.5 mg/dL, or an increase of >50%
over baseline value of serum creatinine or a 50% reduction in estimated GFR

Sodium and potassium balance can be maintained (i.e., urinary excretion equals intake) even
in some patients who have a GFR below 20 mL/min. How might these adaptations occur?

Sodium balance can be maintained as the GFR falls by lowering the rate of tubular
reabsorption. If, for example, the fractional excretion of sodium (FENa) is 0.6% at a normal GFR,
then sodium excretion will remain constant at a GFR that is 20% of normal if the FENa increases
fivefold to 3%. Increased ANP, decreased activity of the renin–angiotensin–aldosterone system,
and pressure natriuresis due to volume expansion-induced hypertension all may contribute to
the decline in sodium reabsorption.

Potassium balance, on the other hand, is maintained by increased collecting tubule potassium
secretion. This process is stimulated by a rise in the plasma potassium concentration and by
aldosterone. Note that the rate of aldosterone release cannot be predicted in renal disease,
since it will tend to be suppressed by volume expansion and enhanced by hyperkalemia.

Consider a patient with underlying renal disease and a baseline plasma creatinine
concentration of 4 mg/dL, which reflects a GFR of 20 mL/min. Assuming no change in
creatinine secretion, what is the approximate new GFR if the plasma creatinine concentration
rises to 6 mg/dL the day after surgery? How are the results different if the plasma creatinine
concentration remains at this level for several days?

The relationship between the plasma creatinine concentration and the GFR can be predicted
only in the steady state when creatinine production and excretion are equal and the plasma
creatinine concentration is stable. The GFR cannot be predicted the day after surgery, since it is
not known if the patient is in a steady state. For example, the GFR could be below 5 mL/min
and the plasma creatinine concentration will continue to rise each day because excretion
remains below the rate of production.

If, however, the plasma creatinine concentration is stable for several days, then the steady
state is present. In this setting, the product of the GFR and the plasma creatinine concentration
must be constant. This product reflects the amount of creatinine filtered and excreted, which,
in the steady state, is equal to the relatively constant amount of creatinine produced. Thus,
20 × 4 = 6 × new GFR New GFR = 13.3 mL/min
A patient with acute renal failure has a urine output of
 1,500 mL/day. Does the relatively
normal urine output exclude the diagnosis of urinary tract obstruction?

In obstruction, as in other renal diseases, the urine output is equal to the difference between
the GFR and tubular reabsorption. Complete obstruction results in no urine output, but the
output is not predictable in patients with partial obstruction. Although the GFR may be
markedly reduced (from elevated tubular pressure), tubular reabsorption also may be
diminished due to both the adaptations described in the answer to Question 1 and tubular
injury induced by the elevated intratubular pressure. Thus, an output of 1,500 mL/day does not
exclude the presence of partial urinary tract obstruction.

In some nephrons, the cellular injury is severe enough to impair sodium reabsorption but not
severe enough to induce back leak. How might reduced sodium chloride reabsorption in the
proximal tubule and loop of Henle contribute to the decline in GFR in ATN? Consider the
mechanisms by which the GFR is normally regulated.

Reduced sodium chloride reabsorption in the proximal tubule and loop of Henle will increase
the delivery of chloride to the macula densa. This will activate the tubuloglomerular feedback
system, which will lower the nephron filtration rate until macula densa delivery has returned
toward nor- mal. If this compensatory decline in GFR did not occur, the reabsorptive capacity of
the distal and collecting tubules might be overwhelmed, leading to potentially fatal sodium and
water losses. Thus, some investigators have called ATN “acute renal success,” since systemic
hemodynamics are preserved