Question

The very high rates of urea transport in the region of the collecting duct in the inner medulla are due to the presence of specific urea transporters that are stimulated by ADH. Suppose you collect urine from two patients who have been deprived of water owernight. One has normally functioning kidneys, and the other has a genetic defect in the urea transporters. How would the two urine samples differ? Explain.

Short answer

In the patient with normally functioning kidneys, ADH stimulates urea transporters, leading to increased urea concentration and more concentrated urine. In contrast, the patient with a genetic defect in urea transporters will have a more dilute urine due to inefficient urea transport and lower urea concentration. The primary difference between the urine samples is the presence of ADH-stimulated urea transport in the patient with normally functioning kidneys.

Step-by-step solution

Understanding the role of ADH and urea transporters

ADH (antidiuretic hormone) is a hormone that plays a significant role in maintaining the body's water balance. It regulates the water reabsorption in the kidneys. When the body needs to conserve water, ADH signals the kidney to reabsorb more water, making the urine more concentrated. Urea transporters are specific proteins in the kidney that facilitate urea transport in the inner medulla. In the presence of ADH, urea transporters are stimulated, leading to higher rates of urea transport.

Urea concentration and functioning urea transporters

In a patient with normally functioning kidneys, ADH will stimulate the urea transporters in the inner medulla, leading to the reabsorption of water and increased urea concentration in the urine. In this case, the urine will be more concentrated because of the higher urea concentration, especially after an overnight water deprivation.

Urea concentration and defective urea transporters

In the other patient, who has a genetic defect in the urea transporters, the ADH may not adequately stimulate the urea transporters in the inner medulla. As a result, the urea transport will not be as efficient, and less water will be reabsorbed by the kidneys, leading to a more dilute urine.

Comparing the two urine samples

Comparing the two urine samples, the one from the patient with normally functioning kidneys will be more concentrated due to the higher urea concentration. The urine sample of the patient with a genetic defect in the urea transporters will be more diluted because of lower urea concentration. The primary difference between the two urine samples would be the presence of ADH-stimulated urea transport in the patient with normally functioning kidneys, leading to a higher urea concentration in their urine.

Key concepts

Antidiuretic Hormone (ADH)

Antidiuretic hormone (ADH), also known as vasopressin, is a critical component in the body's ability to maintain water balance and regulate urine concentration. Produced by the hypothalamus and released by the pituitary gland, ADH targets the kidney's collecting ducts, prompting them to increase water reabsorption back into the bloodstream.

When a person is dehydrated or hasn't consumed water for a period (such as overnight), ADH levels in the bloodstream rise. This hormonal signal triggers the insertion of water channels, called aquaporins, into the membranes of kidney cells, allowing more water to be reabsorbed. Consequently, the volume of urine decreases, and its concentration increases—it becomes more 'concentrated' with solutes like urea.

In the exercise provided, the patient with normal kidney function and ADH activity will produce concentrated urine after water deprivation. The intricate dance between ADH and the kidneys' response is a fine example of the body's homeostatic mechanisms at work.

Urine Concentration

Urine concentration is a measure of how much waste, particularly urea, is dissolved in the water that's excreted by the kidneys. The body's primary method of regulating urine concentration is through the action of ADH and the function of urea transporters.

Urea is a waste product formed from the breakdown of proteins, and its transport out of the blood and into the urine is essential for preventing toxic buildup. ADH increases the permeability of the kidney's collecting ducts not only to water but also to urea, allowing urea to be reabsorbed into the medulla and, later, to be excreted in a highly concentrated form.

Role of Urea in Urine Concentration

Urea itself plays a role in the urine concentration process. By being reabsorbed into the medulla, it creates a gradient that helps to absorb more water from the collecting duct. Thus, normally functioning urea transporters are vital for this concentration gradient. Without adequate urea transport, as seen in the patient with the genetic defect, the gradient is less effective, resulting in less concentrated urine.

Renal Physiology

Renal physiology is the study of kidney function and its role in maintaining the body's internal equilibrium. The kidneys are complex organs responsible for filtering blood, excreting waste products, and balancing levels of electrolytes, among other tasks.

The process of urine formation involves several steps: filtration, reabsorption, secretion, and excretion. During reabsorption, substances the body needs, such as glucose, amino acids, and water, are reabsorbed from the filtrate back into the bloodstream. This process is carefully regulated, and hormones like ADH significantly influence it.

Kidney's Response to ADH

In the context of the exercise, renal physiology explains how urea transporters in the collecting ducts interact with ADH to fine-tune urine concentration. Normally, ADH promotes reabsorption of water by increasing the permeability of the kidney's collecting ducts. In individuals with defective urea transporters, this system cannot work effectively, leading to a disruption in the urine concentration process and, ultimately, the overall renal function. Understanding the interplay between ADH, urea transporters, and the kidneys' structural and functional components is key to grasping renal physiology.