Azotemic or Hydropic Glomerulonephritis

The high concentration of non protein nitrogen (NPN) in the blood of a patient, mainly due to elevated level of urea is termed as azotemia. Elevated level of urea in blood is termed as uremia and it may be due to renal abnormality or due to other health problems like dehydration and excessive burns on the body. The glomerulonephritis (inflammation of glomeruli of kidneys) may be azotemic or hydropic type depending on the nature of glomerular lesions. There may be marked narrowing of the glomerular capillaries leading to azotemia with renal insufficiency and hypertension. On the other hand the status of glomerular capillaries may remain normal but there could be an increase in the permeability of glomerular basement membrane (GBM), the filtration barrier of kidneys. The clinical picture would be hydropic (accumulation of water in the tissues of the body) in character. The hydropic glomerulonephritis is clinically represented with edema associated with hypoproteinemia (low level of protein in blood) and hyperlipemia (high concentration of lipids or cholesterol in blood).

A child or an adult affected with fever or some other acute disease finds the increase in the daily output of urine. There may be tinge of blood in the urine of the patient affected by glomerulonephritis. Sudden appearance of features like puffiness or swelling on face (facial edema), ankles and hands after any acute disease needs expert medical attention and medication. The urine of such patients would show notable excretion of albumin. The patient may be less perspiring with dry skin. The pulse could be full and hard. The loin pain and a feeling of heaviness in the lower abdominal region are the associated symptoms. The polyuria (excessive output of urine) is probably compensatory action of affected kidneys to flush out solid wastes of metabolism form the body. An effective therapy would definitely reverse the associated symptoms and lesions.

How Electrolyte Imbalance Causes Renal Disease Or Renal Disease Leads To Electrolyte Imbalance

Electrolytes or essential ions should always be in the state of homoeostasis. The Normal or standard range of electrolytes reflects the normal functional status of our kidneys. Our kidneys play a vital role in preserving the internal environment while excreting the waste products of metabolism, extra water and electrolytes. There is two way selectivity between the cause and effect between the electrolytes (essential ions) and renal disorder (kidney disease). Depletion of Sodium (Na⁺) or Potassium (K⁺) or Calcium (Ca⁺⁺) through excessive urinary excretion may cause renal failure or renal failure may lead to depletion of these ions or electrolytes in the blood plasma.

The renal tubules play a vital role in regulation and preservation of water and electrolytes. The function of tubular epithelium and tubular enzymes is under the control of hormones of some endocrine glands. Suboptimal response of tubular enzymes or over production of corresponding hormone may cause renal disorder (kidney disease). Anti-diuretic hormone of pituitary gland, aldosterone and parathyroid hormone affect the renal tubules to regulate and preserve the water and electrolytes. Potassium (K⁺) content of the cells plays a critical role in retention or excretion of potassium. The glomeruli of our kidneys excrete Potassium (K⁺) in glomerular filtrate and tubular epithelial cells also excrete Potassium (K⁺) by ion exchange in which Potassium (K⁺) of tubular cells is exchanged by Sodium (Na⁺) of glomerular filtrate. Re-absorption is controlled by proximal tubules whereas the excretion is controlled by distal tubules.

Low dietary intake, fever, trauma, or hemolysis leads to tissue catabolism in patients with anuria (no urine output) leading to release of more Potassium (K⁺) from the cells. In these patients Potassium (K⁺) concentration in blood may reach lethal level (more than 100 mEq/litre). Normal level of Potassium (K⁺) in serum is 5.5 mEq/litre. The clinical features of hyperkalemia (high level of Potassium in blood) could be mainly cardiac (bradycardia or arrhythmia) with significant changes in electrocardiogram (ECG). Potassium (K⁺) depletion may be renal or non-renal in origin and may be suspected when pronounced muscular weakness and lethargy is associated with electrolyte imbalance. Commonest cause of Potassium (K⁺) deficiency could be the uncontrolled use of diuretics for the treatment of congestive heart failure. Potassium (K⁺) deficiency leads to vacuolation of tubular epithelium in proximal tubules (known as clear cell nephropathy). The associated renal changes are reversible with correction in Potassium (K⁺) level in blood/serum. Aldosterone is Sodium (Na⁺) retaining adrenal corticoid secreted by adrenal cortex. Excessive secretion of this corticoid as in cases of adenoma of adrenal cortex may lead to increase in the level of Sodium (Na⁺) and extracellular fluid volume and altered function of Sodium pump. In usual Potassium (K⁺) losing nephropathies there is failure of hydrogen ion excretion in association with the failure of retention or conservation of Potassium (K⁺).

Hypercalcemia (high level of Calcium in blood) as seen in primary hyperparathyroidism, sarcoidosis, excessive vitamin D intake or idiopathic hypercalcemia of infants, may also result in renal damage. Hypercalcemia is also a feature of acute osteoporosis of multiple myeloma and matastatic carcinomatosis of bone. Hypercalcemia could be a lethal complication associated with sarcoidosis but may successfully be reversed with timely steroid therapy. The serum level of Calcium (Ca⁺⁺) may return to normal in a few weeks but the reversal of renal insufficiency may take a year or longer. Calcium (Ca⁺⁺) is retained in our body in the form of Calcium phosphate. The hormone like action of vitamin D during excessive intake, causes increased excretion of phosphorus in urine, unsaturation of serum Calcium phosphate, demineralization of bone leading to increased level of Calcium in blood and increased loss of Calcium in urine. Hypercalcemia could cause nephrocalcinosis leading to renal insufficiency.