Renal parenchyma calcifications

Renal Parenchyma Calcifications By Anthony F. Lalli

R

ENAL PARENCHYMA calcifications, or nephrocalcinosis, may occur as a result of specific lesions within the cortex or medulla or as a consequence of hypercalcemia or hypercalciuria. Papillary nephrocalcinosis is characteristic of hypercalcuric states, whereas with hypercalcemia the calcifications may be more diffusely distributed in the renal cortex and medulla, including the papillae. A number of the diseases that cause nephrocalcinosis are also capable of causing renal calculi; notable among these is primary hyperparathyroidism. One might find it useful to divide the distribution of the renal parenchymal calcifications into those that are cortical and those that are medullary. CORTICAL CALCIFICATIONS

Cortical Necrosis Acute cortical necrosis occurs secondary to ischemic states such as shock, as caused by abruptio placentae, and as a result of exposure to or ingestion of toxins.‘s2 In these conditions focal tubular necrosis usually occurs. The urogram during the acute stage may show an immediate dense and persistent nephrogram. Later, calcification develops within the parenchyma, confined to the cortex (Fig. I), sometimes taking the form of “tram-lines.“’ ’ Acute cortical necrosis is common in patients with acute tubular necrosis and in those with acute pyelonephritis, but is uncommon in other forms of acute renal failure.’ It may be produced by the ingestion of ethylene glycol, an alcohol used as an intoxicant mainly on “skid row,” or by exposure to methoxyflurane.7.8 Both of these materials cause deposition of calcium oxalate or intermediate metabolites, thus damaging the tissues. With methoxyflurane, the fluoride ion may also play a significant part in the tissue destruction.’ Hyperoxaluria

Man cannot metabolize oxalate, and renal excretion is its only route of elimination.” When there is loss of renal function, calcium oxalate crystals may become deposited in the cardiac conduction system, renal parenchyma (Fig. 2A),

Seminars in Roentgenology,

Vol. XVII, No. 2 (April), 1982

joint spaces, blood vessel walls, bone, and elsewhere. Oxalate is the end product of several metabolic pathways.” Hyperoxaluria may result from excess production or intestinal hyperabsorption.‘2 Acquired overproduction of oxalate may follow the ingestion of ethylene glycol or the use of the anesthetic methyoxyflurane. Hereditary hyperoxaluria is a result of deficient enzymes and causes an accelerated conversion of hydroxypyruvate to L-glyceric acid. This leads to oxidation of glycoxalate to oxalate. Gastrointestinal overabsorption of oxalatc, sometimes the result of excessive consumption of rhubarb, is rare. Even in Cincinnati, where bizarre tastes and large patches of rhubarb abound, rhubarb poisoning is uncommon. The colon is the major site of oxalate absorption; in the small intestine the oxalate forms insoluble calcium salts that are nonabsorbable.‘3 Several gastrointestinal disorders are associated with overabsorption of oxalate and hyperoxaluria. These include Crohn disease, celiac sprue, pancreatic insufficiency, and small intestinal bypass surgery for obesity. Dietary fat malabsorption with steatorrhea is common to all these conditions and luminal increase in fatty acids contributes to enhanced absorption. A low fat diet will abolish hyperoxaluria and ileostomy patients do not have it. But patients with jejunocolic or jejunoileal bypasss do. Therefore, excluding the small intestine causes enhanced absorption of oxalate in the colon. Treatment includes reducing the fat and oxalate intake in affected individuals. The renal calcifications in the bowel-shortened patient are primarily medullary and contained in the papillae (Fig. 2B). To the uninitiated eye they may mimic the calcifications of renal tubular acidosis or medullary sponge kidFrom the Clinic Radiology Department, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio. Address reprint requests to Anthony F. Lalli, M.D.. Head, Clinic Radiology Department, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44106 0 I982 hy Grune & Stratton, Inc. 0037 -198X/82/1702-0006$01.00/0

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ney disease. However, the development of the calcification is more rapid, and its extent greater in bypass fistula. Hereditary

Fig. 1. Cortical necrosis following delivery. thin cortical calcifications 3 weeks postpartum. of Dr. Benjamin Felsonj

Note the (Courtesy

Nephritis

(Alport

Syndrome)

Alport syndrome which is also called hereditary nephritis may cause calcification confined to the renal cortex.14 It afflicts males more often than females and is accompanied by recurrent and microscopic hematuria with slow progressive renal failure. Later there is deafness to high frequency sound in 30% to 50% of the patients. The inheritance is autosomal dominant with variable penetrance of X-linked.” The male offspring of affected males do not inherit the disease, but females with the disease transmit it equally to one third to one half of their sons and daughters. The disease is only partially expressed in females but is fully expressed in males.

Fig. 2. Two patients with hyperoxaluria. (A) Homogeneous calcification of the cortex of the left kidney from primary hyperoxaluria. The right kidney had been removed for the same process. Two years later a renal transplant was performed. Calcium oxalate crystals were later deposited in the transplanted kidney as well. iB) Calcium oxelate calculi formed in this patient as a result of small bowel shortening in the treatment of Crohn disease. (Courtesy of Lalli AF: Tailored Urologic Imaging, Year Book Medical Publishers, Chicago, 1981 J

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Fig. 3. calcification Uroradiology Inc.)

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Chronic glomerulonephritis. Renal cortical in a 13-yr-old boy. (Courtesy Cohen L et al: 1980: 2:51-52. Springer-Verlag, NY

The pathologic defect in Alport syndrome may be a disorder of basement membrane synthesis. There may be hematuria for years before the onset of renal failure.16 Males usually die before the fifth decade. Other Causes Cortical glomerulonephritis (Fig. 3),” polycystic disease (Fig. 4), sickle cell disease (most commonly it causes papillary necrosis), Fabry disease, and the nail-patella syndrome are other causes of cortical calcifications. A renal mass with cortical calcification usually proves to be a renal cell carcinoma (Figs. 5 and 6), but may be a simple cyst of the kidney (Fig. 7) or a nephroblastoma (Wilms tumor) (Fig. 8).‘8m20Calcifications are reputed to occur in as many as 20% of renal cell tumors but in fewer than 5% of nephroblastomas. In my experience it is usually the older child or adult with nephroblastoma who will manifest calcifications in the tumor. Neuro-

blastoma calcifies with considerable frequency, in as many as 50% of cases. These calcifications are punctate in form and different from the streaky amorphous calcifications of nephroblastoma (Fig. 9). The calcifications in renal cell carcinoma may be peripheral or central. It is my recommendation to look upon every calcified renal mass with a jaundiced eye, and evaluate it as a possible carcinoma first, although there has been disagreement in the past as to the significance of calcification in a renal carcinoma. When the calcification is present peripherally it usually indicates a less aggressive carcinoma, ie, this is probably an attempt at self-healing.” One may also identify calcified renal artery aneurysm (Fig. 10) or calcified subcapsular hematoma (Fig. I 1) on routine abdominal radiographs. Subcapsular hematoma is usually associated with hypertension. MEDULLARY

Fig. 4. Polycystic kidney disease. Multiple curvilinear calcifications are present in both kidneys on the preliminary film of this 45-yr-old man.

CALFICIATIONS

Hypercalcemia occurs with greatest frequency from dissolution of bone secondary to bony metastases.** It is unusual, however, for this to go on long enough for renal parenchymal calcifications to occur. The most important clinical entity that we should consider in the production of nephrocalcinosis is primary hyperparathyroidism (Fig. 12).23,24In the majority of cases this is a consequence of a single adenoma but it may be the result of diffuse hyperplasia or multiple adenomas.*’ Hyperthyroidism, sarcoidosis, immobilization, especially in young children, and Paget disease are also associated with hypercalcemia and nephrocalcinosis.26 In these conditions the nephrocalcinosis is most commonly medullary, but it may be cortical as well. The other

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Renal cell carcinoma Fig. 5. tion in a large mass in the upper

F. LALLI

with extensive calcificapole of the right kidney.

major causes of predominantly medullary calcinosis are distal renal tubular acidosis and less frequently, the milk-alkali syndrome.27-29 These entities manifest features of hypercalciuria and relatively alkaline urine, which results in the formation of medullary calcium phosphate

Fig. 6. Peripherally calcified renal carcinoma. Note amputation of the calyces in this portion of the kidney. (Courtesy Lalli AF: Tailored Urologic Imaging, Year Book Medical Publishers, Chicago. 1981.)

Fig. 7. Calcified cyst in the upper pole of the left kidney. It proved to be hemorrhagic and fibrous in type. Selective renal angiogram.

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Fig. 8. Left nephroblastoma. Extensive seen throughout the tumor on the plain year-old child. (Courtesy Lalli AF: Tailored ing, Year Book Medical Publishers, Chicago,

calcification is film of this 7Urologic Imag1981.)

Nauroblastoma above the right kidney in an Fig. 9. 18-month-old child. Extensive punctata calcifications are present. (Courtesy Lalli AF: Tailored Urologic Imaging, Year Book Medical Publishers, Chicago, 1981 .I

depositions as well as renal calculi. The radiograph consistently underestimates the amount of calcium deposition which is evident on pathologic examination. The calcification is probably more accurately identified with computerized tomography. The calcification is initially intratubular or intracellular, but subsequently becomes interstitial. The medullary structures, such as the loop of Henle and collecting ducts, are affected first and the proximal and distal convoluted tubules later, presumably because of the higher medullary concentration of the calcium. RENAL TUBULAR ACIDOSIS Fig. 10. Excretory urogram on an asymptomatic patient with rounded peripherally calcified lesion (arrow) in a typical location for aneurysm of the renal artery. (Courtesy Lalli AF: Tailored Urologic Imaging. Year Book Medical Publishers, Chicago, 1981 .I

Renal tubular acidosis is divided neatly into proximal and distal varieties. The proximal form need not concern us as radiologists since it rarely results in nephrocalcinosis or renal calculi.30 It

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Fig. 11. Calcified subcapsular hematoma discovered 10 years after trauma during a football game in a patient with hypertension.

occurs as a result of the suppression of proximal tubule bicarbonate reabsorption which is caused by either an inhibition of the proximal tubular physiologic function or as an intrinsic defect in the proximal tubular hydrogen ion secretion.3’ This condition may coexist or combine with impaired reabsorption of other substances such as glucose, phosphate, amino acids, uric acids, or other organic acids.32In this case, it is known as

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the De Toni-Fanconi syndrome. This euphonious compound eponym is fascinating but is not a radiologic entity. Proximal renal tubular acidosis may also be encountered in adults as a result of the nephrotic syndrome or the ingestion of toxins or drugs. Although the proximal tubule is quantitatively responsible for most of the hydrogen ion secretory capacity of the nephrons, the distal tubule has the unique ability to secrete hydrogen ions against a steep lumenal pH gradient, and thus allows net acid excretion to occur.33S34 When the ability of the distal nephron to lower urinary pH is impaired, several deleterious consequences follow. First there is an escape of bicarbonate even in the face of acidosis, and acid excretion is reduced and hypokalemia occurs due to induced hyperaldosteronism.3s336 Distal renal tubular acidosis may be primary, ie, genetic or idiopathic, or associated with systemic disease,such as Ehlers-Danlos syndrome, sickle cell anemia, thyroiditis, primary hyperparathyroidism, vitamin D intoxication, idiopathic hypercalciuria, medullary spongekidneys, toxic nephropathy from analgesics or cyclamates, chronic pyelonephritis secondary to urolithiasis, and hyperoxaluria. The specific tubular defect in distal renal tubular acidosis is an inability of the distal portion of the nephron to effectively secrete hydrogen ions to lower the urinary pH normally. It is a syndrome characterized by hypokalemic hyperchloremic metabolic acidosis in association with urine that is less than maximally acidotic

Fig. 12. Hyperparathyroidism. Bilateral renal pyramid calcifications are seen on the preliminary film, together with the rather severe osteopenia.

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Fig. 13. Renal tubular acidosis. (A) The preliminary abdominal film of this 36year-old woman uniformly distributed calcifications. (6) The urogrem confirms the papillary location of the calcification.

(pH greater than 5.4). Renal tubular acidosis may be primary or secondary to the antecedent or associated diseases enumerated above. Most cases appear to be sporadic, with no family history. Nephrolithiasis and nephrocalcinosis occur in up to 73% of the primary cases (Fig. 13).17

Medullary Sponge Kidney Disease This is an entity of considerable interest to radiologists. It is also called precalyceal canulicular ectasia. It is generally isolated and nonfamilial, and is usually a silent disease. However, it may present in the fourth to sixth decades of life with renal colic due to the passage of a calculus, microscopic or gross hematuria, or pyelonephritis.38,39The disease may be confined to a single renal unit (Fig. 14) or it may completely involve

Fig. 14. Medullery sponge kidney disease confined to the lower pole of the left kidney. No calcifications were identifiable on the preliminary abdominal examination.

shows

numerous

small

both kidneys (Fig. 15). It is said to be bilateral in 75% of cases. The stones found in this condition contain calcium phosphate, calcium oxalate, or magnesium ammonium phosphate. They are usually tiny (Fig. 16) and the radiologist sees only a fraction of the calculi that are present in the collecting tubules. These may be passed into the collecting system where they may increase in size or be passed down the ureter, causing colic. The disease is generally considered to be benign, but may be debilitating because of numerous episodes of painful colic. The destruction of renal parenchyma that may occur as a result of the superimposed pyelonephritis in the presence of the nephrocalcinosis may become so profound as to result in renal failure and death of the patient. Palubinskas has intensively investigated these patients and has found that the disease may

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Medullary sponge Fig. 15. kidney disease. (A) The preliminary film shows bilateral calcifications. (8) The urographic phase shows extensive bilateral involvement. with many more cavities shown suggested from the number of calcifications.

occur as a forme fruste, manifested only by opacification of the collecting tubules (Fig. 17). This does not appear to progress to the more florid form, in which the cavities or cystic lesions may be seen on the urogram.40*4’ The sine qua non for the diagnosis of this entity is the presence in the urographic phase of more cavities than there are identifiable calculi on the preliminary abdominal film. This constellation of observations does not occur with the other conditions that should be considered in the differential diagnosis, namely renal tuberculosis, papillary necrosis, and renal tubular acidosis. Renal Tuberculosis Of the new cases of tuberculosis currently identified in the United States, 10% are extrapulmonary and the majority of these are genitouri-

nary.42 The kidney is involved early in the course of the disease as a result of a silent bacilluria that occurs during the pulmonary infection.43 These bacteria appear to elicit little in the way of renal parenchymal destruction until years later when the pulmonary lesion has healed and may no longer be identifiable. Tuberculosis probably begins in the cortex and progresses eventually to involve the medullary portions of the kidney, eroding into the collecting system and spreading down the ureter into the bladder. As a rule, it is only when the bladder is involved that the patients become severely symptomatic, as a result of dysuria. Before that the urine may show sterile pyuria or hematuria and the patient may rarely have flank pain. Constitutional symptoms occur in only a fraction of the affected patients. However, the urogram will be

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CALCIFICATIONS

Fig. 16. Medullary sponge kidney disease confined to the left kidney in this patient with numerous calcifications. The right kidney appeared normal on urography.

abnormal in as many as 93% of cases, particularly if it is carefully examined for the small erosions that may occur in the papillae.44 Repeated urine culture will be positive in 90% of affected individuals. Healing results in contraction of the collagen and irregularity, narrowing, and amputation of affected areas, such as the infundibula, ureters, and renal pelves. This is the only bacterial infection of the urinary tract capable of causing amputation or strictures of portions of the upper urinary tract (Fig. 18). Occasionally the entire kidney is destroyed, undergoing s+called autonephrectomy (Fig. 19).

Fig. 17. Forme fruste or incomplete form of medullary with sponge kidney disease blushing of all of the renal pyramids, no calcifications and enlargement of the renal pyramids. There is liile likelihood that this will progress to a clinically manifest form of the disease.

Renal tuberculosis in the upper pole of the Fig. 16. right kidney with amputation of the infundibulum. Calcification was identified on the preliminary abdominal film. (Courtesy Lalli AF: Tailored Urologic Imaging. Year Book Medical Publishers, Chicago, 1961.)

Papillary

Necrosis

Papillary necrosis is most commonly produced by analgesic abuse but may also occur as a complication of sickle cell disease either in the homozygous or heterozygous form, as a result of

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Fig. 19. Autonephrectomy with calcification of the right kidney from longstanding renal tuberculosis. No function has occurred on the urogram. (Courtesy of Dr. Morton Bosniak.)

urinary tract obstruction, or as a complication of diabetes mellitus, and reportedly as a result of alcoholism.4547 As demonstrated by Lindval,48 however, and from our own data,49 most of these patients have accompanying or superimposed pyelonephritis, and one can usefully raise the question as to whether papillary necrosis will occur without accompanying infection. All of the entities associated with its production result in a relative ischemia of the renal papilla. This, of course, would make it particularly vulnerable to

Fig. 20 Calcification

Papillary necrosis (medullary manifested on the preliminary

infection. E. Coli bacteremia probably occurs daily in all of us but is ineffective in the absence of prepared soil where the organisms can flourish.50 The individual who abuses analgesics may prepare that soil. A mixture of aspirin and phenacetin appears to be the most hazardous in producing papillary necrosis, especially when combined with water depletion. This may be particularly prominent in certain cultures and drier climates. The destruction produced may vary from a

necrosis) with extensive destruction of the medullary portion of the kidney. films. (B) Extensive medullary disease is shown best on the urogram.

(A)

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small erosion at the tip of the papillae to involvement of the entire segment of the medulla and even the cortex adjacent to the renal segment (Fig. 20). All of the segments of both kidneys may be involved. Many of the radiologic patterns are difficult if not impossible to distinguish from tuberculosis or medullary sponge kidney disease. One should consistently include the entire trio of these possibilities when one of them is first considered. The retained papillae or bits thereof are likely to calcify and may produce medullary

calcifications on the preliminary abdominal radiograph. If none of the papillae become separated, the radiological diagnosis may be very difficult. Another complication of importance is uroepithelial carcinoma, which is unfortunately common among patients with analgesic nephropathy, and have been said to be as much as 4000 times more frequent than in the general population.52 54

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