Kidney Diseases

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The incidence of serious kidney disease has dramatically increased lately, mostly due to autoimmunity, without any effective treatment.


Kidney damage affects blood flow, glomerular function, tubular function, and abnormal urine composition triggers the development of urinary stones. Kidneys play dominant role in regulation of water, electrolytes, minerals and acid-base balance in the body, and thereby in regulation of blood pressure. Elimination of water and other matter through kidneys is regulated by hormones, i.e. antidiuretic hormone, aldosterone, atrial natriuretic factor, parathormone, calcitriol, calcitonin, cortisol, prostaglandin E2, insulin, estrogens, progesterone, thyroxin, somatostatin.


Blood flow through kidneys is 25% of total. All water in plasma will pass through kidney epithelial cells every 20 minutes, and entire volume of extracellular fluids every 3 hours.


Kidneys produce hormones: calcitriol, rennin-angiotensin, erythropoietin, 40% of insulin breaks down in kidneys, and a significant portion of steroids as well.


Tubular malfunctions:


Genetic defect of kidney and intestinal glucose-galactose transport causes glucose and galactose malabsorption. Genetic defect of another glucose transport protein causes renal glucosuria.


With renal phosphate diabetes the reabsorption of phosphates in decreased which leads to bone demineralization (rachitis). Increased reabsorption of phosphates due to lack of parathormone or disturbance of its effectiveness, i.e. pseudohypoparathyreosis, leads to hyperphosphatemia.


Defect of Na+-co-transport of neutral aminoacids in kidneys and intestine causes Hartnup syndrome with aminoaciduria. Resulting lack of tryptophan leads to the lack of nicotinic acid with damage to CNS and skin.


Defect of aminoacid transport protein for neutral and di-basic aminoacids magnifies losses of ornithin, lysine, arginine, cystin in cystinuria with precipitation of cystin in urine into stones.


Reabsorption of basic aminoacids is disrupted in familial protein intolerance. Defect of co-transport of cyclic aminoacids, i.e. proline, leads to iminoglycinuria.


In acidosis of proximal tubule the reabsorption of HCO3- cannot be balanced out by transport capacity of distal tubule and thereby is excreted in urine even with its normal concentration in plasma.


In Fanconi syndrome several transport systems are malfunctioning, with resulting glycosuria, acidosis of proximal tubule and hypokalemia. We treated a 5 ½ years old boy with otherwise untreatable Debre-De Toni-Fanconi syndrome with fetal cell transplantation of kidney, liver, cartilage, placenta, and mesenchyme. Within 5 months the patient’s height increased by 9 cm, weight by 2.1 kg, waddling gate disappeared, the valgus deformity of the left lower leg decreased. The patient did not have a single respiratory infection that he suffered from regularly. Hypocalcemia and hyperphosphatemia disappeared. Hyperphosphaturia decreased. The urinary calcium excretion became practically normal. Hyperaminoaciduria was substantially decreased. Hepatosplenic syndrome was still present but serum transaminases were dramatically lower. [282]


In gout the excessive Na+ and water reabsorption in proximal tubule concentrates uric acid in the lumen and thereby stimulates its reabsorption with resulting sedimentation of practically insoluble uric acid in joints.


Genetic defect of transport of Cl- or K+ channel is the cause of Bartter syndrome with disrupted urine concentration, natriuresis, hypokalemia, and low blood pressure, despite high levels of rennin, angiotensin, aldosterone.

Genetic defect of transport protein causes Gittelman syndrome, a variant of Bartter syndrome.


Hypoaldosteronism leads to Na+ loss through kidneys, and thereby to lowered volume of extracellular fluid and low blood pressure. Hyperactivity of Na+ channels leads to retention of Na+ and to high blood pressure in Liddle syndrome.


Defect of secretion of H+ in distal tubule leads to acidosis of distal tubule with alkaline urine and frequent calciumphosphate stones.


In rare instances of treatment of Lowe’s oculocerebrorenal syndrome- fetal precursor cell transplantation of kidney, liver, retina, placenta, exocrine pancreas, diencephalon, was used. Water can reabsorb in the entire nephron, with the exception of an ascending Henle loop, but reabsorption in distal tubule and collecting duct requires ADH.


Lack of ADH, or non-responsiveness of nephron to ADH, causes diabetes insipidus, when up to 20 l of hypotonic urine is excreted. Our experience in treatment of central diabetes insipidus by cell transplantation is described in the chapter ‘Genetic diseases.’


All genetic diseases of tubular function of kidneys can be treated with fetal precursor cell transplantation with success.


Glomerular defects:


Glomeruli are damaged by inflammation, i.e. glomerulonephritis, the cause of which are soluble antigen-antibody complexes which deposit onto glomerular basilar membrane and by complement activation trigger local inflammation. This damages glomerular capillaries and destroys filtering, i.e. immunocomplex nephritis. As triggers play part many drugs, allergens, pathogenic microorganisms, especially streptococci group A, and IgG, IgM, IgA as antibodies.


Much less frequent is Matsugi nephritis caused by autoantibodies against basilar membrane with proliferation of endothel, mesangial cells, podocytes, and mesangial matrix.


Glomeruli can be damaged by amyloid deposits in amyloidosis, by high concentration of filtered plasma proteins in plasmacytoma, by high pressure in glomerular capillaries in arterial hypertension, venous thrombosis of renal veins, venous stagnation in right-heart decompensation, hyperfiltration with diabetic nephropathy, as well as by inadequate perfusion in atherosclerosis and arteriolosclerosis.


Facing the fast growing numbers of patients with severe kidney disease the nephrologists would be well advised about BCRO fetal precursor cell transplantation to be used early in the course of nephritis not responding to initial treatmentPatients usually wait before seeking help until after they already began hemodialysis and that is too late. It is well known fact that no patient has ever improved so much after any type of ‘fetal cell transplantation’ to be able to stop a regular hemodialysis! The existing treatments of all degenerative diseases suffer from one common problem: no attempt at regeneration of degenerating cells of diseased organs and tissues is made. The sole treatment available to medicine today to directly regenerate cells, tissues and organs is BCRO type of fetal precursor cell transplantation.. of kidney, adrenal cortex, placenta, artery, mesenchyme, that has been carried out but not reported.


Treatment of pyelonephritis by cell transplantation is contraindicated as it is an inflammatory condition.


Nephrotic syndrome:


Nephrotic syndrome means a syndrome of proteinuria, hypoproteinemia and peripheral edemas. It is the first kidney disease that has been treated with fetal precursor cell transplantation with success already decades ago. A 55 years old female with recurrent asthma developed suddenly swelling of both feet and lower legs with dyspnea, nausea, vomiting, loss of appetite, weakness, so that the patient was confined to bed. The abdominal swelling was increasing, and urinary output minimal. Cell transplantation of placenta, kidney, eliminated most of ascites, restored normal urination, brought back good appetite, within 16 days. [18] Sometimes cell transplants of liver, adrenal cortex, are added.


Glomerular filter, i.e. fenestrated endothel, basilar membrane, podocyte slot membrane, has a selective permeability for various components of blood. Molecules larger than pores cannot pass through filter whatsoever while those smaller than pores pass through equally well as water. Electric charge is very important for permeability: positively charged or neutral molecules pass through the filter much better than negatively charged.


In glomerulonephritis the filter integrity can be broken, so that the access to the cavity of Bowman capsule can be gained not only by proteins but also by erythrocytes. A small transport capacity for proteins cannot ‘keep pace’ with massive quantity of filtered proteins and proteinuria ensues. This leads to hypoproteinemia.


Lipoproteins cannot be filtered even through damaged filter, and since hypoproteinemia stimulates production of lipoproteins in liver, hyperlipidemia develops with hypercholesterolemia.


Hypoproteinemia causes decrease of blood volume, thirst, ADH secretion, aldosterone secretion. Increased water intake and increase of natrium chloride and water reabsorption brings on edema. Aldosteron causes hypokalemic alkalosis.


Interstitial nephritis is an inflammatory kidney disease when inflammation does not originate from glomeruli. The most common form is bacterial nephritis, or pyelonephritis., with involvement of medulla of kidneys, in which due to marked acidity, hypertonicity and ammonia concentration, all defense mechanisms are weakened.


Interstitial nephritis can be caused even without an infection, by deposition of stones of calcium salts, uric acid. Deposits of uric acid in kidney originate from excessive intake of purines in food, but also by excessive endogenous production of uric acid, i.e. after cytostatica for treatment of leukemias. Calcium deposits result from hypercalciuria resulting from increased absorption of calcium in intestine, and excessive calcium mobilization from bones caused by tumors,or immobilization. Infection by urease-splitting microorganism leads to breakdown of urea to ammonia in urine. As ammonia binds hydrogen ions, alkaline urine is produced. This helps phosphate sedimentation, stone production causing disruption of urine outflow and thereby support the development of ascending pyelonephritis, i.e. ‘vitious circle.


In acute kidney failure there is no place for fetal precursor cell transplantation and in chronic kidney failure it is too late: such treatment has not been successful.


Renal hypertension is a direct cause of arterial hypertension in only 7% of patients, but kidneys play the key role in the causation of arterial hypertension and its clinical course, even if there is no kidney disease present. Kidney ischemia leads via stimulation of renin-angiotensin system to arterial hypertension. Retention of sodium and water causes arterial hypertension even without rennin-angiotensin system. Every arterial hypertension cause kidney damage. Ever primary extra-renal hypertension becomes renal hypertension by development of nephrosclerosis.