книги студ / Color Atlas of Pathophysiology (S Silbernagl et al, Thieme 2000)

A. Abnormalities of Urinary Concentration
			Mannitol
Inflammation	Loop diuretics		Excretion of:
				Diabetes insipidus
			glucose,
	Hypercalcemia		urea,	central	renal
Mediators			bicarbonate,
			phosphate
	Hypokalemia			ADH insensitivity
	K+ recirculation		Osmolarity	ADH deficiency		Concentration
Blood
pressure
Caffeine			4			Urinary
			Water reabsorption
						5.5
	ROMK	2	Osmotic diuresis
						Plate
	Na+-K+-2 Cl– cotransport
					1
Vasodilation				Water permeability
3
Perfusion					Protein deficiency
					5
			NaCl and
			urea reabsorption		Urea
	Vasa recta
					Collecting duct
			Loop of
			Henle
	Osmolarity
NaCl	H2O		Urea	Polyuria, nycturia		101

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Abnormalities of Glomerular Function

		The function of the glomeruli is to produce an
		adequate GFR, i.e., the volume of plasma water
		that is controlled by the renal epithelium. The
		selective permeability of this filter (→ p.104)
		ensures the formation of a nearly protein-free
		filtrate. As all of the blood flowing through the
		kidney must pass through the glomerular ves-
	Balance	sels, the resistance of these vessels also deter-
		mines RPF.
		The GFR is determined by the effective fil-
	Water	tration pressure (Peff), the hydraulic conductiv-
		ity (Kf), and the filtering surface		(F): GFR =
		Kf · F · Peff. The effective filtration		pressure is
	and	made up of the hydrostatic (	P) and the oncot-
		ic (Δπ) pressure gradients	across the filter
	Salt	(→ A): Peff = P – Δπ. Even if the filter is defec-
		tive, π within the capsular space of the glomer-
	Kidney,
		ulus can be ignored, i.e., Δπ practically equals
		the plasma oncotic pressure (πcap). As a result
		of glomerular filtration, the protein concentra-
	5	tion in plasma is increased and πcap as a rule

comes close to the hydrostatic pressure gradient toward the end of the glomerular capillary loops (filtration equilibrium).

Reduced hydraulic conductivity (→ A2) or a reduced filtration surface decreases the GFR. No filtration equilibrium can be achieved; as a result of the reduced increase in πcap, Peff ultimately rises. But this does not compensate for the reduced conductivity.

Constriction of the vas afferens (→ A3) when systemic blood pressure remains constant reduces the filtration pressure and thus the proportion of filtered plasma water (filtration fraction = GFR/RPF). At the same time the renal blood flow and the GFR fall because of the increased resistance.

Constriction of the vas efferens (→ A4) raises the effective filtration pressure and thus also GFR/RPF. Simultaneously it reduces glomerular perfusion and thus GFR at any given filtration fraction. The constriction of the vas efferens (e.g., on infusion of angiotensin II) or obstruction of venous flow (e.g., by renal vein thrombosis) can thus ultimately reduce GFR.

The glomeruli can be damaged by inflammatory disease (glomerulonephritis; → B).

102 Among possible causes are soluble antigen– antibody complexes that become entangled in

the glomeruli and, via complement activation, produce local inflammation (→ p. 48ff.). This results in obstruction of the glomerular capillaries and destroys the filtering function (immune complex nephritis). Numerous drugs, allergens, and pathogens can act as antigens. Streptococci (group A, type 12) are very often responsible. Antibodies include IgG, IgM, and commonly IgA (IgA nephritis).

Masugi’s nephritis, caused by autoantibodies against the basement membrane, is much less common than immune complex nephritis. The local inflammation initially results in hyperemia, accumulation of neutrophils (exudative phase), and damage to the often markedly thickened basement membrane. It is common for endothelial, mesangial, or capsular epithelial cells to proliferate and ultimately for excess mesangial matrix to form (sclerosing).

The glomeruli may also be damaged without any local inflammation, for example, by deposition of amyloid in amyloidosis, by a high concentration of filtrable proteins in plasma (e.g., in multiple myeloma), by high pressure in the glomerular capillaries (e.g., in arterial hypertension, renal vein thrombosis, venous back pressure in right heart failure, or hyperfiltration in diabetic nephropathy) as well as by reduced perfusion (e.g., in atherosclerosis, arteriosclerosis).

In glomerulonephritis, resistance in the vasa afferentia and efferentia is increased and the RPF is reduced despite filtration pressure usually being high. The reduced hydraulic conductivity prevents filtration equilibrium being achieved and lowers GFR. The reduced renal perfusion stimulates the release of renin which, via angiotensin and aldosterone, raises blood pressure. In addition, the development of hypertension is aided by reduced excretion of NaCl and H2O, brought about by the decrease in GFR (→ p.114).

Selective permeability is lost by damage to the glomerular filter, thus leading to proteinuria and edema (→ p.104).

Damage to the kidney can, for example, destroy erythropoietin-producing cells and thus result in the development of anemia.

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A. Glomerular Filtration: Vascular Resistance and Hydraulic Conductivity
Glomerulus							Hydraulic
RPF		Normal				RPF	conductivity
a		P			e	a	P	e
Peff			Pressure (kPa)		π
	Capsular space			8			8
					P
GFR normal				4		GFR	4			Function
					Δπ
1						2
				0 a			0 a
						e			e
		Resistance					Resistance			Glomerular
RPF		Vas afferens				RPF	Vas efferens
a		P			e	a	P	e
								πe		5.6
Peff						Peff				Plate
GFR			8			GFR	8
			4				4
3						4
			0 a				0 a
						e			e

B. Glomerular Diseases
Antigen-antibody	Immune complex	Masugi’s	Autoantibodies
complex	nephritis	nephritis
e. g.				e. g.
				Renal vein thrombosis,
Multiple mycloma				venous congestion
Protein concentration				Hydrostatic
in plasma				pressure
Glomerular deposition	Glomerulonephritis			Abnormalities of
of protein				glomerular perfusion
Renal perfusion				Death of
	GFR	Abnormal permselectivity		erythropoietin-
				forming cells
Renin angiotensin		of the glomerular filter
	Hyperhydration
Renal		Proteinuria,		Anemia	103
hypertension		edema
		Photos from: Doerr, W. ed. Organpathologie. Stuttgart: Thieme; 1974

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5 Kidney, Salt and Water Balance

104

Disorders of Glomerular Permselectivity, Nephrotic Syndrome

The glomerular filter (fenestrated endothelium, basement membrane, slit membrane between podocytes) is not equally permeable for all blood constituents (selective permeability or permselectivity). Molecules larger in diameter than the pores do not pass the filter at all. Molecules of clearly smaller diameter will in practice pass through, as will water, i.e., their concentration in the filtrate is approximately the same as that in plasma water. If these substances are not reabsorbed or secreted in the kidney, their clearance (C) is identical to the GFR, and the fractional excretion (C/ GFR) is 1.0. If molecules are only slightly smaller in diameter than the diameter of the pores, only some of them can follow water through the pores, so that their concentration in the filtrate is lower than in plasma (→ A1).

However, permeability is determined not only by the size, but also by the charge of the molecule. Normally, negatively-charged molecules can pass through much less easily than neutral or positively-charged molecules (→ A1). This is due to negative fixed charges that make the passage of negatively-charged particles difficult.

In glomerulonephritis (→ p.102) the integrity of the glomerular filter may be impaired, and plasma proteins and even erythrocytes can gain access to the capsular space (→ A2). This results in proteinuria and hematuria. Close observation of proteinuria indicates that it is especially the permeability for negativelycharged proteins that is increased. This behavior can be demonstrated most impressively by infusing differently charged polysaccharides, because polysaccharides—in contrast to proteins—are hardly reabsorbed by the tubules. Negatively-charged (–) dextrans are normally less well filtered than neutral (n) or cationic (+) dextrans. This selectivity is lost in glomerulonephritis and filtration of negative- ly-charged dextrans is massively increased (→ A2). One of the causes of this is a breakdown of negatively-charged proteoglycans, for example, by lysosomal enzymes from inflammatory cells that split glycosaminoglycan. As has been shown by electrophoresis, it is especially the relatively small, markedly negative- ly-charged albumins that pass across the

membrane (→ A3). Even an intact glomerulus is permeable to a number of proteins that are then reabsorbed in the proximal tubules. The transport capacity is limited, though, and cannot cope with the excessive load of filtered protein at a defective glomerular filter. If tubular protein reabsorption is defective especially small proteins appear in the final urine (tubular proteinuria).

Renal loss of proteins leads to hypoproteinemia. Serum electrophoresis demonstrates that it is largely due to a loss of albumin (→ A4), while the concentration of larger proteins actually tends to increase. This is because the reduced oncotic pressure in the vascular system leads to increased filtration of plasma water in the periphery and thus to a concentration of the other blood constituents. Filtration in the peripheral capillaries is facilitated not only by the reduced oncotic pressure, but also by damage to the capillary wall that may also be subject to inflammatory changes. As a result of protein filtration in the periphery, protein concentration and oncotic pressure rise in the interstitial spaces, so that the filtration balance shifts in favor of the interstitial space (→ A5). If the removal of proteins via the lymphatics is inadequate, edemas form (→ A7).

If proteinuria, hypoproteinemia, and peripheral edema occur together, this is termed nephrotic syndrome. As the lipoproteins are not filtered even if the filter is damaged, but hypoproteinemia stimulates the formation of lipoproteins in the liver, hyperlipidemia results and thus also hypercholesterolemia (→ A6). It remains debatable whether a loss of glomerular lipoprotein lipase contributes to the effect.

Hypoproteinemia favours peripheral filtration, the loss of plasma water into the interstitial space leads to hypovolemia which triggers thirst, release of ADH and, via renin and angiotensin, of aldosterone (→ p.122). Increased water intake and increased reabsorption of sodium chloride and water provide what is needed to maintain the edemas. As aldosterone promotes renal excretion of K+ and H+

(→ p. 98), hypokalemia and alkalosis develop.

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A. Abnormalities of Glomerular Permselectivity and Nephrotic Syndrome

	Normal					Abnormal
1		Glomerular capillary				permselectivity of
						the glomerular filter
		Glomerular filter				2
					Capsular
					space
	1.0						1.0
excretionFractional	0.8			+	Normal	excretionFractional	0.8			Glomerulonephritis
	0.6						0.6	–	+
	0.4		n				0.4
		–
	0.2						0.2
	0		300	360			0	240	300	360	420
	180	240			420		180
		Molecular size (nm)						Molecular size (nm)
		3		Urine					Tubular reabsorption
				electrophoresis
			Albumin		Proteinuria
									Lipoprotein lipase
										deficiency
4		Serum						Lipoprotein			?
		electrophoresis			Hypoproteinemia			synthesis
	Normal
	Albumin	Immunoglobulins			Oncotic pressure in					6
									Hyperlipidemia
					the vascular system
5					decreases				Damage to
									peripheral capillaries

P

Pressure		Filtration	7
			Edema
	π	Resorption

Hypovolemia

Lenght of capillary

ADH

Hypokalemia

Aldosterone

Alkalosis

Plate 5.7 Glomerular Permselectivity: Disorders

105

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5 Kidney, Salt and Water Balance

106

Interstitial Nephritis

The term interstitial nephritis is applied to inflammatory changes in the kidney if the inflammation does not originate in the glomeruli. Renal tissue is infiltrated by inflammatory cells (especially granulocytes) and the inflammation can lead to local destruction of renal tissue.

The most common form of interstitial nephritis is that caused by bacteria (pyelonephritis). Most often the infection originates in the urinary tract (bladder → ureter → kidney [ascending pyelonephritis]); less often in the blood (descending pyelonephritis) (→ A1). The renal medulla is practically always affected first, because its high acidity, tonicity, and ammonia concentration weaken the body’s defense mechanisms. Flushing out the renal medulla thus lowers the danger of infection. Infection is promoted by an obstruction to urinary flow (urinary tract stone [→ p.120], pregnancy [→ p.116], prostatic hypertrophy, tumor) and by reduced immune defenses (e.g., diabetes mellitus [→ p. 290]).

An interstitial nephritis can also cause the deposition of concrements (calcium salts, uric acid) in the renal medulla without any infection (→ A2). Uric acid deposits in the kidney are principally caused by an excessive dietary intake of purines, which are broken down in the body into uric acid, as well as by a massive increase of endogenous uric acid production, as occurs in the leukemias and in rare cases of

enzyme defects of	uric acid	metabolism
(→ p. 250). Calcium	deposits are	the conse-

quence of hypercalciuria that occurs when intestinal absorption of calcium is increased (e.g., in hypervitaminosis D) as well as with increased mobilization of calcium from bone (e.g., by tumors, immobilization; → p.132).

Lastly, interstitial nephritis can result from toxic (e.g., phenacetin) or allergic (e.g., penicillin) factors, from radiation or as a rejection reaction in a transplanted kidney. The renal medulla is especially prone to hypoxia because O2 diffuses from the descending to the ascending limb of the vasa recta. In sickle cell anemia (→ p. 36) deoxygenation therefore leads to precipitation of hemoglobin, especially in the renal medulla, and thus to vascular occlusion.

Massive administration of prostaglandinsynthesis inhibitors can damage the renal medulla by causing ischemia. In normal circumstances renal medullary perfusion at low perfusion pressure is maintained by the release of vasodilating prostaglandins. Inhibition of prostaglandin synthesis stops this protective mechanism, however.

In accordance with the site of the inflammatory processes, the first effects are caused by lesions in the segment of the nephron that lies within the renal medulla (loop of Henle and collecting duct). A relatively early occurrence is reduced urinary concentration, caused by damage to the ascending part, by flushing out of the medulla as a result of inflammatory hyperemia as well as by a lack of sensitivity of the damaged distal nephron to ADH. The increased urine volume causes nocturnal diuresis (nycturia). The decreased K+ secretion into the collecting duct can cause hyperkalemia, while reduced Na+ reabsorption can result in hypovolemia (→ A3). However, the reduced Na+ reabsorption in the loop of Henle can also result in an increased distal K+ secretion with accompanying hypokalemia, especially when more aldosterone is released as the result of hypovolemia (→ p. 266).

Renal acid excretion can be impaired, resulting in an alkaline urine being formed and also in systemic acidosis.

Various functions of the proximal tubules (reabsorption of glucose and amino acids, secretion of PAH) and the glomeruli (GFR) are affected only in advanced pyelonephritis.

Infection by urea-splitting pathogens leads to a breakdown of urea into ammonia in the urine. As ammonia binds hydrogen ions (→ A4), an alkaline urine will result. This promotes the precipitation of phosphate-contain- ing concrements (→ p.120) that in turn can cause obstruction to urinary flow and thus the development of ascending pyelonephritis, i.e., a vicious circle is established.

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A. Interstitial Nephritis
Descending			2
		Deposition of concrements:
pathogens
		calcium salts, uric acid		Toxic damage,
				e. g. phenacetin
				Allergic reaction,
				e. g. penicillin
				Rejection reaction		Nephritis
				after transplantation
		Interstitial nephritis		Inhibitors of
	1
Immune defense				prostaglandin synthesis
						Interstitial
					Ischemia
			Lesions of
			distal nephron			5.8
			3			Plate
Ascending pathogens
					Ca2+
Outflow obstruction					Na+
	O	In			K+
4
		urine
H2N	C	NH2			H+
			Osmotic
CO2			pressure in
			renal medulla
	NH3	H2PO4–
NH4+		H+			H+ secretion
		HPO42–		Systemic
				acidosis	Alkaline urine
Mg2+		Ca2+			Na+ reabsorption
			Impaired urinary
			concentration		Natriuresis
	Precipitation of				K+ secretion
			Hyperkalemia
	phosphate salts					107

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5 Kidney, Salt and Water Balance

108

Acute Renal Failure

Numerous and diverse disorders can lead to more or less sudden impairment of renal function (→ A1):

Obstruction of the urinary tract, for example, by urinary stones (→ p.120) can stop urinary excretion, even though the kidney remains intact—at least at first.

In hemolysis and in the destruction of muscle cells (myolysis) hemoglobin or myoglobin, respectively, is filtered through the glomeruli and precipitated in the acidic tubular lumen, especially because their tubular concentration is increased by fluid absorption. The resulting obstruction leads to urine formation being interrupted.

Renal function can also cease as a result of rapidly progressing renal diseases (e.g., glomerulonephritis; → p.102) or toxic damage to the kidney.

Loss of blood and fluid impairs renal perfusion and glomerular filtration because in centralization of the circulation (→ p. 230) the kidney is treated like a peripheral organ, i.e., sympathetic activation produces renal vascular constriction via α-adrenoceptors. The result is acute ischemic renal failure.

Several pathophysiological mechanisms can prevent the recovery of GFR or restoration of normal excretion of substances filtered by the glomeruli, even after the state of shock has been overcome and blood pressure has been normalized (→ A1):

Constriction of the vasa afferentia:

–Energy deficiency impairs Na+/K+-ATPase;

the resulting increase in intracellular concentration of Na+ also causes, via the 3Na+/ Ca2+ exchanger, a rise in intracellular Ca2+ concentration (→ p.10,12) and thus vasoconstriction.

–The ischemia promotes the release of renin

both primarily and via an increased NaCl supply in the macula densa (reduced Na+ absorption in the ascending tubules) and thus the intrarenal formation of angiotensin II, which has a vasoconstrictor action.

–If there is a lack of energy supply, adenosine is freed from ATP. It acts on the kidney—in contrast to the other organs—as a marked vasoconstrictor.

Obstruction of the glomerular filter by fibrin and erythrocyte aggregates.

Seeping away of filtered fluid in the damaged tubules.

Obstruction of the tubular lumen by desquamated tubular cells, by crystals, or due to swelling of the tubular cells.

Intravascular stasis (“sludge”) that cannot be flushed out of the network between renal medulla and cortex, even if the perfusion pressure rises.

In the first three days of acute renal failure no urine (anuria) or only a little volume of poorly concentrated urine (oliguria) is excreted as a rule (oliguric phase; → A2). However, urinary volume alone is a very poor indicator of the functional capacity of the kidney in acute renal failure, because the tubular transport processes are severely restricted and the reabsorption of filtered fluid is thus reduced. Despite normal-looking urine volume, renal excretion of all those substances that must normally be excreted in the urine may be markedly impaired. In this case determination of the plasma and urine creatinine concentration provides information on the true functional state of the kidneys.

Recovery after the oliguric phase will lead to a polyuric phase characterized by the gradual increase of the GFR while the reabsorption function of the epithelial nephron is still impaired (salt-losing kidney; → A3). If the renal tubules are damaged (e.g., by heavy metals), polyuric renal failure occurs as a primary response, i.e., large volumes of urine are excreted despite a markedly decreased GFR.

The dangers of acute renal failure lie in the inability of the kidney to regulate the water and electrolyte balance. The main threat in the oliguric phase is hyperhydration (especially with infusion of large volumes of fluid) and

hyperkalemia (especially with the simultaneous release of intracellular K+, as in burns,

contusions, hemolysis, etc.). In the polyuric

phase the loss of Na+, water, HCO3–, and especially of K+ may be so large as to be life-threat- ening.

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A. Acute Renal Failure
					Reduced
					renal perfusion,
			Glomerular inflammation,		especially in shock
	1		poisoning, etc.			[Ca2+]
						intracellular
			Fibrin deposition		Vasoconstriction
				GFR
					Renin		Failure
					Angiotensin
		Leak		Adenosine
							Renal
			Obstruction of				Acute
			tubular lumen
						Obstruction	5.9
				Sludge			Plate
	Hypothetic			Ischemia
	mechanism
	(see text)
2
Acute phase		GFR		3
Re-				Secondary phase
absorption						4
					GFR	Recovery
				Re-
				absorption		Reabsorption and GFR
						normalized
Urine volume
100				Oliguria
%
0
100		GFR
%					Polyuria
0
2		14	Days	26
				Hyperhydration,
				hyperkalemia,	Dehydration,
				ascending
					hypokalemia		109
				pyelonephritis

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Chronic Renal Failure: Abnormal Functions

		A number of renal diseases can ultimately lead
		to the destruction of renal tissue (→ p.102ff.,
		114). If the residual renal tissue is not in a posi-
		tion to adequately fulfill its tasks, the picture
		of renal failure evolves.
		Reduced renal excretion is particularly sig-
		nificant. The decreased GFR leads to an in-
	Balance	versely proportional rise in the plasma level
		of creatinine (→ A, top; see also p. 94). The
		plasma concentration of reabsorbed sub-
	Water	stances also rises, but less markedly, because
		renal tubular reabsorption is impaired in renal
		failure. The reabsorption of Na+ and water is
	and	inhibited in renal failure by a variety of factors,
		such as natriuretic hormone, PTH, and van-
	Salt	adate (→ p.112). The reduced reabsorption of
		Na+ in the proximal tubules also directly or in-
	Kidney,	HCO3–, Ca2+, urea, glucose, and amino acids.
		directly decreases the reabsorption of other
		substances, such as phosphate, uric acid,
	5	The reabsorption of phosphate is also inhibited
		by PTH.
		Reduced NaCl reabsorption in the ascending
		limb compromises the concentrating mecha-
		nism (→ p.100). The large supply of volume
		and NaCl from parts of the proximal nephron
		promotes the reabsorption of Na+ distally and
		aids in the secretion of K+ and H+ in the distal
		nephron and in the collecting duct. As a result,
		the plasma concentration of electrolytes can
		remain practically normal even if GFR is mark-
		edly reduced (compensated renal insufficien-
		cy). Disorders occur only once GFR has fallen
		to less than a quarter of the normal level. How-
		ever, this compensation is carried out at the
		cost of the regulatory range, in that the dam-
		aged kidney is unable adequately to increase
		the excretion of water, Na+, K+, H+, phosphate,
		etc. (e.g., if oral intake is increased).
		It is probably the disruption in renal water
		and electrolyte excretion that is responsible,
		at least partially, for the development of most
		of symptoms of chronic renal failure. Excess
		volume and the changed electrolyte concentra-
		tions lead to edemas, hypertension, osteoma-
		lacia, acidosis, pruritus, and arthritis, either di-
		rectly or via the activation of hormones
	110	(→ p.112). Also, abnormalities of the excitato-
		ry cells (polyneuropathy, confusion, coma, sei-
		zures, cerebral edemas), of gastrointestinal

function (nausea, peptic ulcer, diarrhea), and of blood cells (hemolysis, abnormal leukocyte function, abnormal blood clotting) are due to this.

While uric acid can be precipitated at high concentrations, especially in the joints, and thus cause gout (→ p. 250), sufficiently high concentrations of uric acid are only rarely achieved in renal failure. The role of reduced elimination of so-called uremia toxins (e.g., acetone, 2,3-butyleneglycol, guanidinosuccinic acid, methylguanidine, indoles, phenols, aliphatic and aromatic amines, etc.) as well as of so-called middle molecules (lipids or peptides with a molecular weight of 300– 2000 Da) in producing the symptoms of renal failure remains the subject of considerable debate. High concentrations of urea can destabilize proteins and bring about cell shrinkage. But its effect is partly canceled by the cellular uptake of stabilizing osmolytes (especially betaine, glycerophosphorylcholine).

The impaired renal production of erythropoietin leads to the development of renal anemia (→ p. 30ff.), while the reduced formation of calcitriol contributes to abnormalities of mineral metabolism (→ p.112). Depending on the cause and course of the disease, the intrarenal formation of renin and of prostaglandins can be raised (→ p.114) or reduced (death of reninor prostaglandin-producing cells). Increased formation of renin promotes, while its reduced formation inhibits, the development of hypertension, a frequent occurrence in renal failure (→ p.112ff.). Prostaglandins, on the other hand, are more likely to cause vasodilation and a fall in blood pressure (→ p. 296). The loss of renal inactivation of hormones

(→ p. 92) may slow down hormonal regulatory cycles. It is not clear, however, what the role of these changes is in the development of symptoms.

The reduced consumption of fatty acids by the kidney contributes to hyperlipidemia, while reduced gluconeogenesis favors the development of hypoglycemia.

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