STUDY - Technical - New Dacian's Medicine
The Main
Manifestations of Kidney Disease (2)
Translation Draft
As we announced yesterday, "start" but postrenal nitrogenemia.
As we announced yesterday, "start" but postrenal nitrogenemia.
Urinary tract obstruction
is responsible for less than 5% of cases of acute renal failure,
but is usually reversible and should be excluded at the
beginning of the evaluation. Because a single kidney is able to
maintain adequate clearance, acute renal failure by obstruction
requires either obstruction of the urethra or bladder or
bilateral ureters, or unilateral obstruction in a patient with a
single functional kidney.
Obstruction is usually diagnosed by the presence of ureteral dilation in renal ultrasound. However, at the beginning of the evolution of the obstruction or if the ureters cannot dilate (such as their encasedness in a pelvic tumor), the ultrasound may be negative.
Oliguria refers to a urinary flow of less than 500 ml in 24 hours, and anuria is the complete absence of urine formation. Anuria can be caused by total obstruction of the urinary tract, total occlusion of the arteries or renal veins and shock (manifested by severe hypotension and intense renal vasoconstriction). Cortical necrosis, NTA and rapidly progressive glomerulonephritis can occasionally cause anuria. Oliguria can accompany any cause of renal failure in all situations except prerenal nitrogenemia.
Nonoliguria refers to a urinary flow of more than 500 ml/ day in patients with acute or chronic nitrogenemia. In nonoliguric NTA, disturbances in the potassium and hydrogen balance are less severe than in oligurian patients, and the return to normal renal function is usually rapid.
It's time to "talk" about urine abnormalities, and I'll start with proteinuria. Large amounts of plasma proteins normally pass through the glomerular capillaries but do not enter the urinary space. Selectivity of both load and size virtually prevents albumin, globulins and other high molecular weight proteins from being crossed through the glomerular wall.
Smaller proteins penetrate the capillary wall, but are easily re-orbited by the proximal tube. Most individuals excrete between 30 and 150 mg/ day of total protein (normal upper limit being 200 mg/ day) and only about 30 mg/ day of albumin. The rest of the protein in the urine is secreted by tubi (Tam-Horsfall, IgA and urokinase) or represent small amounts of beta 2 globulins, apoproteins, enzymes and filtered peptic hormones. Tubular proteinuria due to proteins of low molecular weight occurs in diseases that harm the tubes more than glomerules. The resulting proteinuria is usually between 1 and 3 g/ day, only with small amounts of albumin present.
Current methods of measuring proteinuria vary significantly. Determination with dipstick detects mostly albumin and gives false positive results when the pH is greater than 7 (basic urine) and urine is highly concentrated or contaminated with blood. A highly diluted urine can hide a significant proteinuria on the dipstick. Tests for accurate measurement of total urinary concentration are based on precipitation with sulfosalicylic or tricloracetic acid. Dipsticks that measure microalbuminuria (30 to 200 mg/ l), an early marker of glomerular diseases, are currently available.
Normal glomerular endothelial cells form a barrier, penetrated by windows of about 100 nm, which retains cells and other particles but is a minor impediment to the passage of most proteins. The glomerular basal membrane stops most large proteins while extensions of epithelial cells (podocytes) cover the urinary slope of the glomerular basal membrane and produce a series of narrow channels (cleaved diaphragms) that allow the molecular passage of small solvents and water.
The channels are lined with glycoproteins that are rich in glutamate, aspartate and sialic acid and are negatively charged to physiological pH. This negatively charged barrier prevents the passage of anionic molecules such as albumin. Glomerular diseases can interrupt the basal membrane by storing immune complexes, allowing the leakage of large proteins. Several glomerular diseases mainly affect epithelial cells and result in the loss of podocyte and consecutive albuminuria extensions. When total daily protein excretion (mostly albumins) exceeds 3.5 g, hypoalbuminemia, hyperlipidemia and edema (nephrotic syndrome) are often associated.
However, in some plasmocyte cell discs (such as multiple myeloma) a total protein urinary excretion of more than 3.5 g/ day occurs, without other features of nephrotic syndrome. These diseases can be associated with large amounts of light chains excreted in the urine, which cannot be detected by dipsticks, which detect especially albumin. The light chains produced in these diseases are filtered by glomerules and exceed the reabsorption capacity of the proximal tube.
A precipitate of sulfosalicylic acid that is disproportionate to the estimates on the analysis dipstick is suggestive of light chains (the Bence-Jones protein), and the typical light chains are re-dissolved when the precipitate is warmed. Renal failure in these diseases occurs through a variety of mechanisms including tubular obstruction (cylindrical nephropathy) and storage of light chains.
Hypoalbuminemia from nephrotic syndrome occurs from excessive urinary loss, increased renal catabolism and inadequate hepatic synthesis. The resulting decrease in plasma oncotic pressure contributes to the formation of edema by altering Starling forces and favoring the movement of fluid from the capillaries to the interstitial. The resulting homeostatic mechanisms, intended to correct the decrease in effective intravascular volume, contribute to the formation of edema.
These mechanisms include activation of the renin-angiotensin system, AVP and sympathetic nervous system, which contribute to excessive renal reabsorption of salt and water and can contribute to the inevitable edema. The severity of edema correlates with the degree of hypoalbuminemia and is altered by other factors, such as heart disease or peripheral vascular diseases. Low plasma oncotic pressure and urinary loss of regulating proteins seem to stimulate hepatic lipoprotein synthesis. The resulting hyperlipidemia has the effect of the appearance of lipid bodies in the urine (fat cylinders, oval fatty bodies).
Other proteins are lost in the urine leading to a variety of metabolic disorders, including globulin binding to tyrotoxin, the protein that binds cholecalciferol, transferin and proteins that bind metals. A state of hypercoagulability frequently accompanies severe nephrotic syndromes due to urinary loss of antithrombin III, low serum levels of S and C proteins, hyperfibrinogenemia and increased platelet aggregation. Some patients develop severe IgG deficiencies with consecutive immunity defects.
I will now present some elements about hematuria, piuria and cylinders. Isolated hematuria without proteinuria, other cells or cylinders is often an indicator of bleeding from the urinary tract. Hematuria is defined as the presence of two to five erythrocytes in the high-strength microscopic field and can be detected with dipsticks. Common causes of isolated hematuria include calculus, neoplasms, tuberculosis, trauma and prostatitis. Macroscopic hematuria with blood clots is almost never an indicator of glomerular bleeding, but rather suggests a postrenal source in the urinary collector system.
A single urine test showing hematuria is common and may be the result of menstruation, viral diseases, allergy, physical exertion or mild trauma. However, persistent or significant hematuria (greater than three high-strength microscopic field erythrocytes at three different analyses or a single analysis with more than 100 erythrocytes or macroscopic hematuria) identifies significant renal or urological lesions. Even patients receiving chronic anticoagulant treatment should be investigated.
Hematuria with pyuria and bacteria is typical for infection and should be treated with antibiotics after adequate cultivation. Acute cystitis or acute urethritis in women can cause microscopic hematuria. Hypercalciuria and hyperuricosuria are also risk factors for unexplained isolated hematuria in both children and adults. In some of these patients (50-60%), reducing calcium and uric acid excretion through diet interventions can eliminate microscopic hematuria. Isolated microscopic hematuria can be a manifestation of glomerular diseases.
Erythrocytes of glomerular origin are often dysmorphic on microscopic examination with phase contrast. Irregular forms of erythrocytes may also occur due to changes in pH and osmolarity in the distal tube. However, there is significant variability among observers in the detection of dysmorphic erythrocytes, especially if they do not have a phase contrast microscope. The most common etiologies of isolated glomerular hematuria are IgA nephropathy, hereditary nephritis and thin basal membrane disease. Nephropathy but IgA and hereditary nephritis may present episodic macroscopic hematuria.
A family history of renal failure is often present in patients with hereditary nephritis, and patients with thin basal membrane disease often have other family members with microscopic hematuria. A renal biopsy is required for the definitive diagnosis of these diseases. hematuria with dysmorphic erythrocytes, erythrocyte cylinders and protein excretion greater than 500 mg/ day is virtually diagnosed for glomerulonephritis. Erythrocytic cylinders form as erythrocytes enter the tubular fluid and are trapped in a cast of Tamm-Horsfall gelatinous proteins.
Even in the absence of nitrogenemia, these patients should undergo serological evaluation and renal biopsy. Isolated piuria is rare because inflammatory reactions in the kidneys or collector system are associated with hematuria. The presence of bacteria suggests infection, and leukocyte cylinders alongside bacteria are indicators of pyelonephritis. Leukocytes and/ or leukocyte cylinders can be seen in tubulointestithial processes such as interstitial nephritis, systemic lupus erythematosus and transplant rejection. In chronic kidney diseases, degenerate cell cylinders called cero cylinders can be seen in urine. Large cylinders are believed to occur in dilated tubes of enlarged nephrons, which have suffered compensatory hypertrophy in response to reduced renal mass (i.e. chronic renal failure). A mixture of large cylinders along with cell cylinders and erythrocytes can be seen in insidious conditions, such as chronic glomerulonephritis with persistent active glomerulitis.
I will complete this post with the presentation of urinary volume abnormalities. The reduced urine volume varies depending on fluid intake, renal function and physiological needs of the individual. The causes of low urination production (oliguria) or absence (anuria) have been discussed in previous posts. As for polyuria (high urinary production) there are a few things to present. Only from history, it is often difficult to tell the frequency of urination (often small volumes) of polyuria (for evaluation it is necessary to collect urine on 24 hours). It is necessary to determine whether polyuria is an osmotic or aqueous diuresis and whether diuresis is appropriate to clinical circumstances.
An ordinary person excretes between 600 and 800 mosm of solvents daily, mainly as urea and electrolytes. Urinary osmolarity can help distinguish osmotic diuresis from aqueous diuresis. If the urinary flow is greater than 3l/ day (arbitrarily defined as polyuria) and the urine is diluted (less than 260 mosm/ l) then the total excretion of milliosmoli (mosm) is normal and an aqueous diuresis is present. This may occur in polydipsia, inadequate secretion of AVP (central insipid diabetes) or inability of renal tubules to respond to AVP (nephrogen insipid diabetes).
If the urinary volume is more than 3 l/day and the urinary osmolarity is greater than 300 mosm/l, then osmotic diuresis is clearly present and the search for responsible solvent(s) is mandatory. Excessive filtration of a hard-reabsorbable solvent such as glucose or urea can inhibit the reabsorption of salt (NaCl) and water into the proximal tube and lead to increased urinary excretion. Poorly controlled diabetes is the most common cause of osmotic diuresis, leading to volemic dresion and serum hypertonia.
Because the urinary concentration of sodium is lower than that of blood, more water is lost than Na, causing hypernatremia and hypertonia. Iatrogenic osmotic diuresis usually occurs after administration of mannitol, radiological contrast substances and protein-rich diet (enteral and parenteral), leading to increased urea production and excretion. Less commonly, excessive sodium loss may occur in renal cystic diseases and Bartter syndrome or during the development of a tubulointerstitial process (such as acute tubular necrosis in resolution). In these so-called salt-loss diseases, tubular lesions result in direct alteration of Na reabsorption and indirectly reduce the tube response to aldosterone. Usually, Na losses are small and mandatory urine excretion is less than 2 l/ day. Acute tubular necrosis in remission and post-obstructive diuresis are exceptions and may be associated with significant natriarezis and polyuria.
The formation of large diluted urine volumes are polydipsic statuses or insipid diabetes. Primary polydipsia may be the result of habits, mental illness, neurological damage or medication. During deliberate polydipsia, the volume of extracellular fluid is normal or increased, and AVP levels are low, as serum osmolarity tends to be close to the lower limits of normal.
The reabsorption of water from distal contorted tubes and collecting tubes is minimal when AVP levels are low. The stimulus for water reabsorption is also low due to the "washing" of medullary hypertonicity gradients. Serum na concentration may help distinguish patients with primary polydipsia from those with insipid diabetes (patients with polydipsia tend to have low or normal serum concentrations, while patients with insipid diabetes usually have normal to high concentrations). A water deprivation test may be required to specify the exact diagnosis.
Central insipid diabetes may have idiopathic origin or may be secondary to a variety of hypothalamic conditions including post-hypophysectomy status, traumatic, neoplastic, inflammatory, vascular or infectious hypothalamic diseases. Idiopathic central insipid diabetes is associated with selective destruction of neurons that secrete vasopressin from the supraoptic and paraventricular core and can be inherited as a predominant autosomal trait or may occur spontaneously. Nephrogen insipid diabetes can occur in a variety of clinical situations. Hypercalcemia and hyperpotasemia are reversible causes of nephrogenic insipid diabetes, but there are also familial conditions.
Usually, nephrogen insipid diabetes is acquired as a result of kidney disease or drug treatment. In both central and nephrogenic insipid diabetes, water reabsorption is reduced along the distal nephron. Similar to the washing of medullary gradients observed in polydipsia, insipid diabetes is associated with dilution of medullary solvents. AVP administration may lead to the formation of more concentrated urine, but the maximum urinary osmolarity achieved is often below normal. Determining plasma AVP levels is recommended as the best method for distinguishing central insipid diabetes from nephrogenic diabetes. Alternatively, a water deprivation test and exogenous administration of AVP may differ primary polydipsia from central and nephrogenic insipid diabetes.
Tomorrow I should present to you some "stuff" about disorders of motion, incontinence and bladder pain, and the day after tomorrow about fluid and electrolyte imbalances (part one, because these imbalances require a higher number of posts). If the fun at sea doesn't give me time... Hmmm, you realize they're going to be on duty and I'm going to get... So,
A restful and/ or fun weekend, full of understanding, love and gratitude!
Obstruction is usually diagnosed by the presence of ureteral dilation in renal ultrasound. However, at the beginning of the evolution of the obstruction or if the ureters cannot dilate (such as their encasedness in a pelvic tumor), the ultrasound may be negative.
Oliguria refers to a urinary flow of less than 500 ml in 24 hours, and anuria is the complete absence of urine formation. Anuria can be caused by total obstruction of the urinary tract, total occlusion of the arteries or renal veins and shock (manifested by severe hypotension and intense renal vasoconstriction). Cortical necrosis, NTA and rapidly progressive glomerulonephritis can occasionally cause anuria. Oliguria can accompany any cause of renal failure in all situations except prerenal nitrogenemia.
Nonoliguria refers to a urinary flow of more than 500 ml/ day in patients with acute or chronic nitrogenemia. In nonoliguric NTA, disturbances in the potassium and hydrogen balance are less severe than in oligurian patients, and the return to normal renal function is usually rapid.
It's time to "talk" about urine abnormalities, and I'll start with proteinuria. Large amounts of plasma proteins normally pass through the glomerular capillaries but do not enter the urinary space. Selectivity of both load and size virtually prevents albumin, globulins and other high molecular weight proteins from being crossed through the glomerular wall.
Smaller proteins penetrate the capillary wall, but are easily re-orbited by the proximal tube. Most individuals excrete between 30 and 150 mg/ day of total protein (normal upper limit being 200 mg/ day) and only about 30 mg/ day of albumin. The rest of the protein in the urine is secreted by tubi (Tam-Horsfall, IgA and urokinase) or represent small amounts of beta 2 globulins, apoproteins, enzymes and filtered peptic hormones. Tubular proteinuria due to proteins of low molecular weight occurs in diseases that harm the tubes more than glomerules. The resulting proteinuria is usually between 1 and 3 g/ day, only with small amounts of albumin present.
Current methods of measuring proteinuria vary significantly. Determination with dipstick detects mostly albumin and gives false positive results when the pH is greater than 7 (basic urine) and urine is highly concentrated or contaminated with blood. A highly diluted urine can hide a significant proteinuria on the dipstick. Tests for accurate measurement of total urinary concentration are based on precipitation with sulfosalicylic or tricloracetic acid. Dipsticks that measure microalbuminuria (30 to 200 mg/ l), an early marker of glomerular diseases, are currently available.
Normal glomerular endothelial cells form a barrier, penetrated by windows of about 100 nm, which retains cells and other particles but is a minor impediment to the passage of most proteins. The glomerular basal membrane stops most large proteins while extensions of epithelial cells (podocytes) cover the urinary slope of the glomerular basal membrane and produce a series of narrow channels (cleaved diaphragms) that allow the molecular passage of small solvents and water.
The channels are lined with glycoproteins that are rich in glutamate, aspartate and sialic acid and are negatively charged to physiological pH. This negatively charged barrier prevents the passage of anionic molecules such as albumin. Glomerular diseases can interrupt the basal membrane by storing immune complexes, allowing the leakage of large proteins. Several glomerular diseases mainly affect epithelial cells and result in the loss of podocyte and consecutive albuminuria extensions. When total daily protein excretion (mostly albumins) exceeds 3.5 g, hypoalbuminemia, hyperlipidemia and edema (nephrotic syndrome) are often associated.
However, in some plasmocyte cell discs (such as multiple myeloma) a total protein urinary excretion of more than 3.5 g/ day occurs, without other features of nephrotic syndrome. These diseases can be associated with large amounts of light chains excreted in the urine, which cannot be detected by dipsticks, which detect especially albumin. The light chains produced in these diseases are filtered by glomerules and exceed the reabsorption capacity of the proximal tube.
A precipitate of sulfosalicylic acid that is disproportionate to the estimates on the analysis dipstick is suggestive of light chains (the Bence-Jones protein), and the typical light chains are re-dissolved when the precipitate is warmed. Renal failure in these diseases occurs through a variety of mechanisms including tubular obstruction (cylindrical nephropathy) and storage of light chains.
Hypoalbuminemia from nephrotic syndrome occurs from excessive urinary loss, increased renal catabolism and inadequate hepatic synthesis. The resulting decrease in plasma oncotic pressure contributes to the formation of edema by altering Starling forces and favoring the movement of fluid from the capillaries to the interstitial. The resulting homeostatic mechanisms, intended to correct the decrease in effective intravascular volume, contribute to the formation of edema.
These mechanisms include activation of the renin-angiotensin system, AVP and sympathetic nervous system, which contribute to excessive renal reabsorption of salt and water and can contribute to the inevitable edema. The severity of edema correlates with the degree of hypoalbuminemia and is altered by other factors, such as heart disease or peripheral vascular diseases. Low plasma oncotic pressure and urinary loss of regulating proteins seem to stimulate hepatic lipoprotein synthesis. The resulting hyperlipidemia has the effect of the appearance of lipid bodies in the urine (fat cylinders, oval fatty bodies).
Other proteins are lost in the urine leading to a variety of metabolic disorders, including globulin binding to tyrotoxin, the protein that binds cholecalciferol, transferin and proteins that bind metals. A state of hypercoagulability frequently accompanies severe nephrotic syndromes due to urinary loss of antithrombin III, low serum levels of S and C proteins, hyperfibrinogenemia and increased platelet aggregation. Some patients develop severe IgG deficiencies with consecutive immunity defects.
I will now present some elements about hematuria, piuria and cylinders. Isolated hematuria without proteinuria, other cells or cylinders is often an indicator of bleeding from the urinary tract. Hematuria is defined as the presence of two to five erythrocytes in the high-strength microscopic field and can be detected with dipsticks. Common causes of isolated hematuria include calculus, neoplasms, tuberculosis, trauma and prostatitis. Macroscopic hematuria with blood clots is almost never an indicator of glomerular bleeding, but rather suggests a postrenal source in the urinary collector system.
A single urine test showing hematuria is common and may be the result of menstruation, viral diseases, allergy, physical exertion or mild trauma. However, persistent or significant hematuria (greater than three high-strength microscopic field erythrocytes at three different analyses or a single analysis with more than 100 erythrocytes or macroscopic hematuria) identifies significant renal or urological lesions. Even patients receiving chronic anticoagulant treatment should be investigated.
Hematuria with pyuria and bacteria is typical for infection and should be treated with antibiotics after adequate cultivation. Acute cystitis or acute urethritis in women can cause microscopic hematuria. Hypercalciuria and hyperuricosuria are also risk factors for unexplained isolated hematuria in both children and adults. In some of these patients (50-60%), reducing calcium and uric acid excretion through diet interventions can eliminate microscopic hematuria. Isolated microscopic hematuria can be a manifestation of glomerular diseases.
Erythrocytes of glomerular origin are often dysmorphic on microscopic examination with phase contrast. Irregular forms of erythrocytes may also occur due to changes in pH and osmolarity in the distal tube. However, there is significant variability among observers in the detection of dysmorphic erythrocytes, especially if they do not have a phase contrast microscope. The most common etiologies of isolated glomerular hematuria are IgA nephropathy, hereditary nephritis and thin basal membrane disease. Nephropathy but IgA and hereditary nephritis may present episodic macroscopic hematuria.
A family history of renal failure is often present in patients with hereditary nephritis, and patients with thin basal membrane disease often have other family members with microscopic hematuria. A renal biopsy is required for the definitive diagnosis of these diseases. hematuria with dysmorphic erythrocytes, erythrocyte cylinders and protein excretion greater than 500 mg/ day is virtually diagnosed for glomerulonephritis. Erythrocytic cylinders form as erythrocytes enter the tubular fluid and are trapped in a cast of Tamm-Horsfall gelatinous proteins.
Even in the absence of nitrogenemia, these patients should undergo serological evaluation and renal biopsy. Isolated piuria is rare because inflammatory reactions in the kidneys or collector system are associated with hematuria. The presence of bacteria suggests infection, and leukocyte cylinders alongside bacteria are indicators of pyelonephritis. Leukocytes and/ or leukocyte cylinders can be seen in tubulointestithial processes such as interstitial nephritis, systemic lupus erythematosus and transplant rejection. In chronic kidney diseases, degenerate cell cylinders called cero cylinders can be seen in urine. Large cylinders are believed to occur in dilated tubes of enlarged nephrons, which have suffered compensatory hypertrophy in response to reduced renal mass (i.e. chronic renal failure). A mixture of large cylinders along with cell cylinders and erythrocytes can be seen in insidious conditions, such as chronic glomerulonephritis with persistent active glomerulitis.
I will complete this post with the presentation of urinary volume abnormalities. The reduced urine volume varies depending on fluid intake, renal function and physiological needs of the individual. The causes of low urination production (oliguria) or absence (anuria) have been discussed in previous posts. As for polyuria (high urinary production) there are a few things to present. Only from history, it is often difficult to tell the frequency of urination (often small volumes) of polyuria (for evaluation it is necessary to collect urine on 24 hours). It is necessary to determine whether polyuria is an osmotic or aqueous diuresis and whether diuresis is appropriate to clinical circumstances.
An ordinary person excretes between 600 and 800 mosm of solvents daily, mainly as urea and electrolytes. Urinary osmolarity can help distinguish osmotic diuresis from aqueous diuresis. If the urinary flow is greater than 3l/ day (arbitrarily defined as polyuria) and the urine is diluted (less than 260 mosm/ l) then the total excretion of milliosmoli (mosm) is normal and an aqueous diuresis is present. This may occur in polydipsia, inadequate secretion of AVP (central insipid diabetes) or inability of renal tubules to respond to AVP (nephrogen insipid diabetes).
If the urinary volume is more than 3 l/day and the urinary osmolarity is greater than 300 mosm/l, then osmotic diuresis is clearly present and the search for responsible solvent(s) is mandatory. Excessive filtration of a hard-reabsorbable solvent such as glucose or urea can inhibit the reabsorption of salt (NaCl) and water into the proximal tube and lead to increased urinary excretion. Poorly controlled diabetes is the most common cause of osmotic diuresis, leading to volemic dresion and serum hypertonia.
Because the urinary concentration of sodium is lower than that of blood, more water is lost than Na, causing hypernatremia and hypertonia. Iatrogenic osmotic diuresis usually occurs after administration of mannitol, radiological contrast substances and protein-rich diet (enteral and parenteral), leading to increased urea production and excretion. Less commonly, excessive sodium loss may occur in renal cystic diseases and Bartter syndrome or during the development of a tubulointerstitial process (such as acute tubular necrosis in resolution). In these so-called salt-loss diseases, tubular lesions result in direct alteration of Na reabsorption and indirectly reduce the tube response to aldosterone. Usually, Na losses are small and mandatory urine excretion is less than 2 l/ day. Acute tubular necrosis in remission and post-obstructive diuresis are exceptions and may be associated with significant natriarezis and polyuria.
The formation of large diluted urine volumes are polydipsic statuses or insipid diabetes. Primary polydipsia may be the result of habits, mental illness, neurological damage or medication. During deliberate polydipsia, the volume of extracellular fluid is normal or increased, and AVP levels are low, as serum osmolarity tends to be close to the lower limits of normal.
The reabsorption of water from distal contorted tubes and collecting tubes is minimal when AVP levels are low. The stimulus for water reabsorption is also low due to the "washing" of medullary hypertonicity gradients. Serum na concentration may help distinguish patients with primary polydipsia from those with insipid diabetes (patients with polydipsia tend to have low or normal serum concentrations, while patients with insipid diabetes usually have normal to high concentrations). A water deprivation test may be required to specify the exact diagnosis.
Central insipid diabetes may have idiopathic origin or may be secondary to a variety of hypothalamic conditions including post-hypophysectomy status, traumatic, neoplastic, inflammatory, vascular or infectious hypothalamic diseases. Idiopathic central insipid diabetes is associated with selective destruction of neurons that secrete vasopressin from the supraoptic and paraventricular core and can be inherited as a predominant autosomal trait or may occur spontaneously. Nephrogen insipid diabetes can occur in a variety of clinical situations. Hypercalcemia and hyperpotasemia are reversible causes of nephrogenic insipid diabetes, but there are also familial conditions.
Usually, nephrogen insipid diabetes is acquired as a result of kidney disease or drug treatment. In both central and nephrogenic insipid diabetes, water reabsorption is reduced along the distal nephron. Similar to the washing of medullary gradients observed in polydipsia, insipid diabetes is associated with dilution of medullary solvents. AVP administration may lead to the formation of more concentrated urine, but the maximum urinary osmolarity achieved is often below normal. Determining plasma AVP levels is recommended as the best method for distinguishing central insipid diabetes from nephrogenic diabetes. Alternatively, a water deprivation test and exogenous administration of AVP may differ primary polydipsia from central and nephrogenic insipid diabetes.
Tomorrow I should present to you some "stuff" about disorders of motion, incontinence and bladder pain, and the day after tomorrow about fluid and electrolyte imbalances (part one, because these imbalances require a higher number of posts). If the fun at sea doesn't give me time... Hmmm, you realize they're going to be on duty and I'm going to get... So,
A restful and/ or fun weekend, full of understanding, love and gratitude!
Dorin, Merticaru