Block 6 Renal Physiology BRS W Expl Prt 1

An acid pH, together with decreased HCO3- and decreased PCO2, is consistent with metabolic acidosis with respiratory compensation (hyperventilation). Diarrhea causes gastrointestinal (GI) loss of HCO 3--, creating a metabolic acidosis.

Glomerular filtration will stop when the net ultrafiltration pressure across the glomerular capillary is zero; that is, when the force that favors filtration (47 mm Hg) exactly equals the forces that oppose filtration (10 mm Hg + 37 mm Hg).

Dilation of the afferent arteriole will increase both renal plasma flow (RPF) [because renal vascular resistance is decreased] and glomerular filtration rate (GFR) [because glomerular capillary hydrostatic pressure is increased]. Dilation of the efferent arteriole will increase RPF, but decrease GFR. Constriction of the efferent arteriole will decrease RPF (due to increased renal vascular resistance) and increase GFR. Both hyperproteinemia (inc  in the glomerular capillaries) and a ureteral stone (inc hydrostatic pressure in Bowman's space) will oppose filtration and decrease GFR.

At concentrations greater than at the transport maximum (Tm) for glucose, the carriers are saturated so that the reabsorption rate no longer matches the filtration rate. The difference is excreted in the urine. As the plasma glucose concentration increases, the excretion of glucose increases. When it is greater than the T m, the renal vein glucose concentration will be less than the renal artery concentration because some glucose is being excreted in urine and therefore is not returned to the blood. The clearance of glucose is zero at
concentrations lower than at Tm (or lower than threshold) when all of the filtered glucose is reabsorbed, but is greater than zero at concentrations greater than Tm.

The person with water deprivation will have a higher plasma osmolarity and higher circulating levels of antidiuretic hormone (ADH). These effects will increase the rate of H20 reabsorption in the collecting ducts and create a negative freewater clearance (- CH20). Tubular fluid/plasma (TF/P) osmolarity in the proximal tubule is not affected by ADH.

After drinking distilled water, subject A will have an increase in intracellular fluid (ICF) and extracellular fluid (ECF) volumes, a decrease in plasma osmolarity, a suppression of antidiuretic hormone (ADH) secretion, and a positive free-water clearance (CH2O), and will produce dilute urine with a high flow rate. Subject B, after drinking the same volume of isotonic NaCl, will have an increase in ECF volume only and no change in plasma osmolarity. Because subject B's ADH will not be suppressed, he will have a higher urine osmolarity, a lower urine flow rate, and a lower C H2O than subject A.

Distal K+ secretion is decreased by factors that decrease the driving force for passive diffusion of K + across the luminal membrane. Because spironolactone is an aldosterone antagonist, it reduces K+ secretion. Alkalosis, a diet high in K +, and hyperaldosteronism all increase [K +] in the distal cells and thereby increase K+ secretion. Thiazide diuretics increase flow through the distal tubule and dilute the luminal [K +] so that the driving force for K+ secretion is increased.

To answer this question, calculate the glomerular filtration rate (GFR) and C. GFR = 150 mg/ml x 1 ml/min / 1 mg/m1= 150 ml/min. C. = 100 mg/ml x 1 ml/min / 2 mg/ml = 50 ml/min. Because the clearance of X is less than the clearance of inulin (or GFR), net reabsorption of X must have occurred. Clearance data alone cannot determine whether there has also been secretion of X. Because GFR cannot be measured with a substance that is reabsorbed, X would not be suitable.

The Henderson-Hasselbalch equation can be used to calculate the ratio of HA/A-:
pH = pK + log A-/HA
7.4 = 5.4 + log A-/HA
2.0 = log A-/HA
100 = A-/HA or HA/A- is 1/100

Mannitol is a marker substance for the extracellular fluid (ECF) volume.
ECF volume = amount of mannitol/concentration of mannitol = 1 g - 0.2 g/0.08 g/L = 10 L.

Increasing filtration fraction means that a larger portion of the renal plasma flow (RPF) is filtered across the glomerular capillaries. This increased flow causes an increase in the protein concentration and oncotic pressure of the blood leaving the glomerular capillaries. This blood becomes the peritubular capillary blood supply. The increased oncotic pressure in the peritubular capillary blood is a driving force favoring reabsorption in the proximal tubule. Extracellular fluid (ECF) volume expansion, decreased peritubular capillary protein concentration, and increased peritubular capillary hydrostatic pressure all inhibit proximal reabsorption. Oxygen deprivation would also inhibit reabsorption by stopping the Na+-K+ pump in the basolateral membranes.

A person who produces hyperosmotic urine (1000 mOsra/L) will have a negative free-water clearance (-C H20) [ CH2O = V - Cosm]. All of the others will have a positive CH20 because they are producing hyposmofic urine as a result of the suppression of antidiuretic hormone (ADH) by water drinking, central diabetes insipidus, or nephrogenic diabetes insipidus.

Total daily production of fixed H + from catabolism of proteins and phospholipids (plus any additional fixed H+ that is ingested) must be matched by the sum of excretion of H+ as titratable acid plus NH 4+ to maintain acid-base balance.

At plasma concentrations that are lower than at the transport maximum (Tm) for para-aminohippuric acid (PAH) secretion, PAH concentration in the renal vein is nearly zero because the sum of filtration plus secretion removes virtually all PAH from the renal plasma. Thus, the PAH concentration in the renal vein is less than that in the renal artery because most of the PAH entering the kidney is excreted in urine. PAH clearance is greater than inulin clearance because PAH is filtered and secreted; inulin is only filtered.

The decreased arterial [1-1CO 3-] is caused by gastrointestinal (GI) loss of HCO 3- from diarrhea, not by buffering of excess H ± by HCO3-. The woman is hyperventilating as respiratory compensation for metabolic acidosis. Her hypokalemia cannot be the result of the exchange of intracellular H + for extracellular K+ , because she has an increase in extracellular H ±, which would drive the exchange in the other direction. Her circulating levels of aldosterone would be increased as a result of extracellular fluid (ECF) volume contraction, which leads to increased K + secretion by the distal tubule and hypokalemia.

Decreases in arterial PCO2 cause a decrease in the reabsorption of filtered HCO3- by diminishing the supply of H + in the cell for secretion into the lumen. Reabsorption of filtered HCO3- is nearly 100% of the filtered load and requires carbonic anhydrase in the brush border to convert filtered HCO 3- to CO2 to proceed normally. This process causes little acidification of the urine and is not linked to net excretion of H + as titratable acid or NH4+.

Interstitial fluid volume is measured indirectly by determining the difference between extracellular fluid (ECF) volume and plasma volume. Inulin, a large fructose polymer that is restricted to the extracellular space, is a marker for ECF volume. Radioactive albumin is a marker for plasma volume.