OVERVIEW
Hypokalemic nephropathy is a potassium-losing nephropathy caused by chronic hypokalemia. Increased urinary potassium excretion from various causes is the most important cause of hypokalemia, collectively known as nephrogenic hypokalemia. In addition to hypokalemia, patients often suffer from metabolic acidosis or metabolic alkalosis. Most patients with hypokalemia with metabolic acidosis have normal blood pressure, while most patients with hypokalemia with metabolic alkalosis have hypertension.
Etiology
The main causes of hyperkalemia include: insufficient potassium intake; excessive loss (from the digestive tract and in the urine); various diuretics and steroid hormone applications; chronic renal diseases such as renal tubular acidosis, Bartter’s syndrome, Liddle’s syndrome, nephrin-secreting tumors, Cushing’s syndrome, and hydroxylase-deficiency diseases. Non-nephrogenic hypokalemia does not increase renal excretion of potassium; increased cellular uptake of potassium due to various reasons is also a common cause of hypokalemia.
Symptoms
Hypokalemic nephropathy is mainly manifested by renal tubular function damage, with reduced concentrating function as the main manifestation, which is characterized by irritable thirst, polydrinking, polyuria, increased nocturia, and even nephrogenic uremic dysuria, and poor response to pressurization; urine is accompanied by a small amount of proteinuria and tubular phenotype; loss of potassium can lead to metabolic alkalosis; and after renal mesangium is damaged, metabolic acidosis occurs because of the dysfunction of renal tubular acidification. The disease is easily complicated by pyelonephritis, with clinical manifestations of urinary tract infection; chronic renal insufficiency gradually appears with the progression of the disease. In addition to the symptoms of renal disease, the patient’s systemic manifestations mainly include hypokalemia, such as muscle weakness of limbs, intestinal paralysis, flaccid paralysis, weakened tendon reflexes, cardiac arrhythmia, and so on.
Examination
1. Urine examination
Urine protein and tubular pattern can be seen, and more leukocytes can be seen when complicated with infection. Urine concentration and dilution test shows decreased concentration function, decreased specific gravity of urine (decreased excretion rate of phenol red and p-aminomalonic acid), and increased urinary prostaglandin E.
2. Blood tests
Blood creatinine and urea nitrogen may be normal in the early stage of the disease; when renal failure occurs with the progression of the disease, blood creatinine and urea nitrogen levels increase. The characteristic change is the decrease of blood potassium, often accompanied by hypochloremia. Blood gas analysis suggests metabolic alkalosis.
3. Renal biopsy and imaging tests
The characteristic structural changes associated with potassium loss are vacuolated degeneration of the tubular epithelium, renal interstitial inflammation and fibrosis, and tubular cystic lesions.
Diagnosis
The diagnosis of the disease may be considered if there is a clinically significant etiology of potassium loss and typical clinical and laboratory manifestations of renal tubular involvement.
Treatment
Hypokalemic nephropathy is caused by hypokalemia, so treatment for hypokalemia is the most fundamental treatment. Since the consequences of hypokalemia are serious if not corrected in time, the general principle of treatment must be mastered, i.e., to remove the cause of hypokalemia. Hypokalemia caused by redistribution of intracellular and extracellular potassium ions for various reasons is generally transient, and to a lesser extent does not require treatment, but if the hypokalemia is more serious, potassium supplementation is necessary. Oral potassium chloride can be given for less severe hypokalemia. For long-term potassium supplementation, extended-release forms of KCl may be given, as KCl extended-release tablets reduce gastrointestinal irritation and fluctuations in blood potassium concentration. Intravenous potassium supplementation, with potassium chloride being the most commonly used, should be given to patients with severe potassium deficiency or those who are unable to take it orally for reasons such as fasting. In patients with hypokalemia associated with hyperchlorhydria, potassium chloride should not be used to replenish potassium if there are obvious signs of renal tubular acidosis, except in emergencies, when non-chlorinated potassium salts are generally preferred. For patients with oliguria, especially those with potassium-preserving diuretics, overkill and hyperkalemia should be borne in mind when supplementing potassium. On the contrary, patients with metabolic acidosis may further aggravate hypokalemia when correcting acidosis, so the dose and rate of potassium supplementation should be increased accordingly.